In childhood, the foundations for health are laid for the rest of your life. This is a very important period in the formation of the body, and vitamins play an important role in the growth process. Moms and dads should be attentive to their baby’s vitamin diet. For quite a long time, mother's milk replaces the child's entire varied diet. Milk contains absolutely all the substances a little person needs in the first months of life. But later, the baby needs a wider range of nutrients.

Starting from about a year, when the baby’s diet is more similar to the usual food of an adult, mothers have to think more about the correct balance of vitamins. Food needs to be varied, then the supply of biologically active substances will be carried out in the required quantities and proportions. The basis of the vitamin diet from 1 year to 16 years are vitamins A, C and D. However, others, of course, are also needed by a growing person. For example, vitamin C is poorly absorbed without the “support” of vitamin R. And in case of hypervitaminosis, which is caused by an overdose of one biologically active substance, sometimes the help of some other substance is very effective.

From the age of 1 to 3 years, the body needs nutrients that primarily promote active growth. During this period, weight increases significantly, the skeleton is strengthened, and muscle tissue grows. The most important vitamins for a child are A, D1 and D2, C and K.

Vitamin A (retinol) contributes to normal metabolism, growth and development of the body. It is also needed to combat various infectious diseases. A source of vitamin A is carrots. This statement is not entirely true. Carrots contain provitamin A - carotene, which is converted into retinol already in the digestive tract. Potatoes are also rich in provitamin A, especially varieties with yellow flesh. Apples mainly supply iron, but they are also quite high in vitamins A, C and B1.

Vitamins of group D are responsible for the absorption of calcium. In their absence, children develop rickets, a disease in which softening of the bone tissue, curvature of the limbs and chest, growths on the skull. In addition, vitamin D deficiency leads to late or, conversely, premature teething, various dental diseases, and tooth loss.

Excellent supplier of calciferol – fish fat, a useful but not very pleasant product. In this case, you can always give fish oil with a tasty bun. In addition to food, sunlight is also a source of vitamin D. Ultraviolet rays convert cholesterol into calciferol. In order for the level of vitamin D in the body to be normal, in the summer the baby must sunbathe a little.

Ascorbic acid, or vitamin C, is perhaps indispensable at any stage of development. It very effectively protects a person from all infectious diseases. In the period from 1 year to 3 years, infections are a serious enemy of babies. In addition, vitamin C promotes better carbohydrate metabolism and is responsible for blood clotting.

Vitamin K also has a good effect on blood health. Its deficiency leads to increased bleeding, and the ability of muscle tissue to regenerate decreases.

At this stage, many diseases specific to this age sometimes develop. Vitamins B3 and B6 take an active part in the fight against them, helping to eliminate allergic reactions. Doctors often prescribe B6 in the form medicinal product(pyridoxine hydrochloride) for diathesis. A serious disease such as polio is treated with vitamin B1.

The vitamin complex, which promotes active growth and normal functioning of the optic nerves, includes such biologically active substances as vitamins A, B2, B6, C, H, B8.

The effect of vitamins A and C on a child has already been discussed. Vitamins B2 and B6 activate metabolism, especially proteins, and are thus responsible for the growth and development of a small person. As a result of a deficiency of these substances, the mucous membranes of the eyes, lips, tongue, nose, ears can be affected, growth can be inhibited, and the processes of brain formation can be disrupted.

Vitamin H (biotin) is highly effective in terms of growth. It is involved in fat metabolism and activates activity nervous system. Scientists have found that if there is a lack of biotin, the body's growth may stop. Sometimes biotin deficiency leads to hair loss and even baldness. Vitamin B8 has similar properties.

Changing baby teeth still requires large portions of vitamin D. At this age, bone formation also continues, so proper regulation of phosphorus and calcium is important.

Botkin's disease is quite common in children. Its consequences are eliminated by increased consumption of vitamin K, which regulates liver function and promotes better blood clotting.

The distribution of vitamins in a schoolchild's diet should be very thoughtful. First of all, you need to include in his diet vitamin complex, helping to restore strength after heavy physical and mental stress. This complex includes all the same basic biologically active substances: vitamins A, B1, C, P.

At school, the strain on the eyes increases greatly: children read, write, and prepare homework. Moreover, now the younger generation spends a lot of time in front of computer monitors. Vitamins A, B1, B2, B6 help strengthen eye muscles And better work optic nerve.

But if vitamin A, as well as carotene (provitamin A) protect to a greater extent from night blindness, B1 and B6 affect the condition of the mucous membrane of the eyes, then vitamin B2 promotes visual acuity. B2 (riboflavin) is prescribed for conjunctivitis and clouding of the cornea of ​​the eyes, sometimes it is used in the form of eye drops that help relieve fatigue from excessive eye strain. Riboflavin is a highly effective remedy for improving vision and preventing color blindness. It is often used for increased eye strain. The source of vitamin B2 is milk and dairy products.

Vitamin B1 acts as a regulator of the activity of the cardiovascular and nervous systems. It promotes the absorption of glucose, without which normal functioning of the heart is simply impossible. Vitamin PP helps strengthen the walls of blood vessels and has the ability to expand the lumens of capillaries.

At this age, sexual function actively develops. Vitamin E (tocopherol) is prescribed by doctors for instability of the menstrual cycle, which is often observed in teenage girls. Tocopherol is responsible for the production of hormones and the development of reproductive function. In addition, vitamin E works well for muscular dystrophy, including a positive effect on the functioning of the heart muscle.

The table below shows the optimal intake of vitamins in adolescence, adulthood and old age. Remember that after the 15-16 year mark, all processes in the body have much greater individuality than in childhood. If all 5-year-old or 10-year-old children have basically the same age characteristics and develop at more or less the same speed, then later this pattern is broken. For some people, life processes begin to wind down very gradually; such individuals remain cheerful and healthy for many years. Others age quickly. Therefore, the age divisions given in the table should be considered rather conditionally. To the greatest extent this concerns the border separating mature age from the elderly.

The already mentioned vitamin B1 (ribovit) will help cope with overload on the visual organs. Protein, carbohydrate and fat metabolism also depend on it. Metabolic disorders can occur at any age. The content of ribovit is quite high not only in meat, but also in cereals, especially in oatmeal and bread (rye or wholemeal).

Vitamin C is a kind of universal vitamin, responsible for almost all functions. In cases of increased mental and physical activity The need for it is growing sharply.

At this age, vitamins A and E are still important. Vitamin A, in addition to already listed functions, promotes the normal condition of the skin. For young people aged 16 to 25, skin often becomes the number one problem: for some it is flaky from dryness, for others it is shiny from oil. Therefore, vitamin A must be constantly supplied to the body in the required quantities. Vitamin E promotes the deposition of vitamin A in the liver, normalizes protein, fat and mineral metabolism.

Vitamins are still very important for normal functioning. Between the ages of 25 and 50, hematopoietic disorders and problems associated with excess cholesterol are common. Sometimes it is during this period that diseases of neuralgic origin develop.

Vitamins B12 (cyanocobalamin) and Bc (folic acid) successfully cope with hematopoiesis problems. They act in partnership, as one complements the functions of the other. Vitamin B12 ensures normal maturation of red blood cells and stimulates the process of hematopoiesis in the bone marrow. In addition, it has a beneficial effect on the functioning of the heart muscle and the thyroid gland. Sun (in some sources this vitamin is also called B9) plays an important role in the prevention of fatty liver and atherosclerosis.

The source of vitamin B12 is not only animal food, but also plant food, such as beets. This product has a very high cobalt content, which is used by the intestinal microflora for the synthesis of cyanocobalamin.

Vitamins such as B3 and B15 are responsible for removing various toxic substances from the body. They regulate the functions of the liver and adrenal glands. Preparations containing these substances are prescribed for alcohol or drug poisoning. B3 and B15 are present in foods such as green peas, eggs, beef liver and kidneys.

Vitamin E (tocopherol) is very important for the normal functioning of the reproductive system. Its ability to positively influence menstrual cycle women. But for men it is one of the most necessary. Tocopherol is responsible for potency.

A pregnant woman's need for vitamins increases sharply. Many physiological processes are rebuilt, obeying the need to bear a fetus. For the proper functioning of such processes, additional portions of biologically active substances are required.

As can be seen from the table above, the diet of pregnant women should contain almost all vitamins, but the presence of some of them is especially important.

Thus, vitamin B3 is one of the most effective helpers in the fight against toxicosis. It relieves allergic reactions, regulates the functions of the adrenal glands and thyroid gland. B3 helps remove excess moisture from the body, but puffiness is serious problem for many pregnant women. It also has a good effect on the skin and relieves dermatitis. A pregnant woman needs to cleanse her body of toxins and neutralize the effects of taking medications. In these cases, vitamin B3 helps very effectively: it neutralizes many harmful substances that accumulate in the liver.

Vitamin B6 plays a big role in regulating proper metabolism. It also helps eliminate symptoms of toxicosis in pregnant women, cope with insomnia or, conversely, drowsiness. B6 is also important for the normal functioning of the nervous system. A woman needs vitamins B3 and B6 primarily in the early stages of pregnancy.

Another B vitamin is Bc (B9, or folic acid). Its deficiency entails disruption of normal hematopoiesis. Deficiency often occurs in the body of pregnant women folic acid and, as a result, anemia develops. To do this, you need to eat liver and fresh parsley from time to time.

In order for the unborn child to have a properly formed skeleton, a pregnant woman should eat more foods containing vitamins D1 and D2.

A pregnant woman’s body absolutely needs tocopherol; it helps preserve the fetus. Vitamin E is prescribed by doctors in cases where there is a real threat of spontaneous abortion or when previous pregnancies have already ended in miscarriages. A nursing mother also needs vitamin E - it helps restore the menstrual cycle after childbirth. A lot of tocopherol is contained in vegetable oils, primarily in soybean and cotton.

The presence of vitamin K in the diet is especially important in the last stages of pregnancy. It is involved in blood clotting and prevents various types of bleeding, including nosebleeds, hemorrhoids and other bleeding in newborns.

The final part of the vitamin complex for pregnant and lactating women is, of course, vitamin C. Without it, any person weakens, his immunity decreases, and the likelihood of various infectious diseases increases.

With age, many vital functions of our body are disrupted, and various diseases arise. After 50 years (some earlier, some later), hormonal levels change, and the speed of vital processes slows down. Therefore, people who have crossed the 50-year mark need to rebuild their nutrition system, giving up some foods in favor of others, and, accordingly, change the amount of vitamins they consume.

From this point of view, it is difficult to overestimate the importance of vitamin B1. Thiamine deficiency can cause a stroke - sudden disturbance activity of the central nervous system (CNS), since it is B1 that most influences its normal functioning. Thiamine is responsible for the metabolism of carbohydrates, which are necessary for the functioning of the central nervous system.

In old age, it is important to prevent an excess of vitamin A in the body. Since this vitamin tends to accumulate, its excess can cause symptoms such as peeling skin and excessive drowsiness.

Atherosclerosis, which occurs due to the deposition of cholesterol on the walls of blood vessels, can also be effectively treated with vitamins B6 and B15. They help remove excess fat from the body and help dissolve cholesterol.

B13 is a fairly rare vitamin found in milk, dairy products, liver, and yeast. It is very useful for older people, as it effectively dissolves cholesterol.

Vitamin F performs a similar function; its deficiency leads to thrombosis. Vitamin F converts cholesterol into a soluble form - this is the only way it can be removed from the body.

Vitamin PP (nicotinic acid) is also very useful for the prevention and treatment of vascular diseases. PP has a vasodilating effect and nourishes tissue cells with hydrogen.

Radish is good for preventing diseases associated with excess cholesterol, gastritis and peptic ulcers. It has an excellent effect on digestive function, stimulating the secretion of gastric juice and activating blood circulation in the walls of the stomach and intestines. This simple and common food product contains a very high concentration of vitamins C and B1, which actively influence a person’s vitality.

To all of the above about atherosclerosis, it remains to be added that after 50 years you should be very careful with the consumption of drugs that are high in vitamin D. These are, for example, calciferol, ergocalciferol (vitamins D2), as well as oxidevit (vitamin D3). The fact is that these substances have a toxic effect and tend to accumulate in the body. They can settle on the walls of blood vessels, forming so-called atherosclerotic plaques.

Vitamin U is an antiulcer factor. It is found in vegetables, primarily cabbage and potatoes. With its help, stomach and duodenal ulcers are perfectly cured.

By the way, regular white cabbage contains many beneficial substances. There are also valuable B vitamins: B1, B2, B3, and vitamins P, PP, K, and, of course, U. In addition, cabbage contains quite a lot of vitamin C.

Liver diseases lead to the accumulation of poisons in the body and disruption of hematopoietic function. Vitamin B4 is largely responsible for the normal functioning of this vital organ. Choline, as it is also called, prevents fatty liver and is responsible for normal blood production. B4 promotes the removal of poisons and relieves us of toxic substances.

The complex of vitamins that successfully resist various liver diseases also includes B15, B6, B13 and vitamin F.

Our list of vitamins that are most important in old age is completed by tocopherol, or vitamin E. We have already talked about it more than once beneficial properties. Tocopherol normalizes oxidative processes, which is also very important for older people.

For normal life, animals need to receive from food, in addition to proteins, fats, carbohydrates, salts and water, additional substances known as vitamins. The main purpose of vitamins is to regulate the biochemical processes that underlie the construction of organic matter in tissues from nutrients supplied with food. Most vitamins perform their regulatory role in assimilation processes through the enzymes in which they are included. Lack or absence of vitamins leads to the cessation of the synthesis of various enzymes and disruption of the processes regulated by them.

Vitamin A (retinol). Vitamin A is one of the fat-soluble nutritional factors necessary for animals to maintain the normal structure of the epithelial, nervous and other tissues of the body and provides a number of vital physiological functions - growth, reproduction, vision. Vitamin A deficiency in the body of animals leads primarily to a disorder of reproductive ability. In females in this case, pathological changes in the development of follicles during the process of ovulation, impaired implantation, death and resorption of a significant part of the fetuses at different stages of their development are observed. As a result, many females are left without offspring and the number of puppies in the litters of females that give birth is much lower than usual.

Puppies from vitamin A-deficient females are born weak, nonviable, and with reduced resistance to infection. Epithelial metaplasia and dryness of the mucous membranes that occur with vitamin A deficiency reduce their barrier functions against infection and

contribute to the development of pulmonary and gastrointestinal diseases among the young.

In male animals, vitamin A deficiency causes deviations in the structure of the testes, the state of the germinal epithelium and seminiferous tubules, as a result of which sperm production is impaired, the quality of the semen deteriorates and sexual potency decreases.

Pereldik and Argutinskaya (1948), who studied the effect of vitamin A deficiency on the reproductive functions of minks, showed that pre-rutting feeding with food deficient in vitamin A for 5 months caused azospermia in males, and the same feeding for 2 months resulted in a decrease in sperm activity almost half. Among females that received little vitamin A during the breeding season (from December to April), the number of those who were missing increased to 70%, and the fertility of females that gave birth decreased by 1.5-2 times.

The clinical picture of A-vitaminosis caused experimentally in fox puppies was described by Smith (1941). The earliest signs of deficiency, which appeared in the 2-3rd month after depriving the puppies of the vitamin, were nervous phenomena: twitching (shaking) of the head, abnormal throwing it back, circling around the cage, lack of coordination of movements, nervous seizures.

Keratinization of the epithelium in the trachea, bronchi, renal pelvis, as well as xerophthalmia (dry eyes) developed in fox puppies later - at 5-8 months.

Vitamin A deficiency is usually accompanied by suppressed growth and increased mortality of puppies. The fallen were found to have inflammation of the mucous membranes of the stomach, intestines and urinary tract, often with ulcerations. Urinary stones are often found in the kidneys and bladder.

In mink puppies, vitamin A deficiency clinically manifests itself in much the same way as in fox puppies. In them, the first signs of vitamin deficiency were established after 58 days of feeding with food deficient in vitamin A (Bassett, 196I).

The results of a generalization of the practice of feeding minks in a number of fur farms and Lebedeva’s own research (1962) gave grounds to believe that a deficiency of vitamin A in diets is often the main cause of urolithiasis in minks.

Regular and sufficient supply of young animals with vitamin A during the growth period is important not only to ensure their intensive growth and obtain large-sized skins, but also for better development of winter hairline and normal formation of sexual functions in replacement young animals. With small doses of vitamin, the hair of animals, especially minks, loses its shine, becomes dull, and the reproductive qualities of breeding young animals deteriorate.

The minimum requirement of silver-black foxes for vitamin A is, according to Smith (1942), Bassett et al. (1948), 25 IU, or 7.5 mcg per 1 kg of live weight. Fox puppies given these doses of the vitamin showed no signs of deficiency and grew normally.

The minimum requirement of young minks for vitamin A turned out to be slightly higher than that of foxes. Bassett (1961) managed to prevent the occurrence of deficiency in minks only by giving 100 IU of the vitamin per 1 kg of live weight. At a daily dose of 25 IU per 1 kg of live weight, mink puppies showed signs of vitamin deficiency on the 84th day of feeding.

As a result of the analysis of feeding in the best production; Based on farm indicators, we have established that in order to ensure normal reproduction of all types of animals, it is necessary to give vitamin A 3 times more than the minimum dose during periods of preparation for the rut, pregnancy and lactation. The best results for the yield of young animals, their preservation and growth were recorded with a daily supply of 250 ME or more per 1 kg of live weight of females. In this case, a significant accumulation of vitamin B was achieved. liver of puppies. Vitamin A supplements, which exceed 10 times the minimum dose, are justified in practical conditions in that they level out existing fluctuations in the need and metabolism of the vitamin depending on the state of the body, the nature of nutrition and other conditions.

The concentration of the vitamin also drops as a result of liver damage from alkaloids, toxins, and worms.

Vitamin E (tocopherols) protects vitamin A from oxidation in the intestinal canal and thereby promotes its better absorption. Tocopherol also has a protective effect against vitamin A in all tissues of the body. This explains the rapid depletion of vitamin A reserves from the liver of animals when fed fats with a high content of unsaturated fatty acids, leading to depletion of the body in vitamin E. It has also been established that animals use vitamin A better when vitamin C is given along with it.

Animals are able to accumulate vitamin A in the liver, kidneys and other organs and gradually use it up.

With long-term feeding of sea fish, whale, beef liver, fish oil and other sources of vitamin A, its concentration in the liver of animals can reach 10 mg or more (more than 33 thousand ME) per 1 g of liver.

Ahman. (1967), feeding mink puppies with different amounts of cod fat and beef liver, established a linear relationship between the accumulation of vitamin A in the liver of animals and its content in food, regardless of the sources of the vitamin.

Due to the ability of animals to create reserves of vitamin A in the body, it can be given once every 3-5 days, but in large doses. True, in this case, retinol is used somewhat worse than with daily dachas.

Diets of animals, in which the group of animal feed mainly consists of meat by-products (without liver), fish meal, skim milk, are often deficient in vitamin A, and the introduction of supplements of this vitamin into such diets has a beneficial effect on productivity.

Animals fed with sea fish and fish waste (with entrails) in the amount of 25-30% of the protein given to them fully satisfy their need for vitamin A. In experiments carried out at the Research Institute of Fur Farming and Rabbit Breeding in 1976-1977 gg. Adding vitamin A to mink diets with whole pollock (30%) had no effect on growth or reproductive performance compared to mink fed the same diets but without vitamin A supplementation. Only when fed cooked or canned fish, and fish after long-term storage at temperatures above -18 °C, diets may not contain enough vitamin A to meet the animals’ need for it.

Vitamin A is easily oxidized in the presence of oxygen, especially at high temperatures. It is very sensitive to various oxidizing agents - salts of iron, copper, zinc and other metals. Rancid fats have a destructive effect on vitamin A. When feed with oxidized fat is included in the feed mixture, a significant part of the vitamin A contained in the mixture is destroyed.

When cooking feed in closed vessels, the loss of vitamin is insignificant.

The reserves of vitamin A in the animal body are concentrated mainly in the liver, therefore, on fur farms, a selective study of the liver of animals slaughtered before the rut to establish the degree of vitamin A supply of the herd has justified itself. The detected deposition of vitamin A in the liver indicates the saturation of the body with the vitamin.

Ahman (1971) reported that when a mink puppy was given 225 to 270 IU of vitamin A per day for 5 months from July 15, vitamin A was found in the liver of the puppies in the range of 100-300 IU, or an average of 160 IU, per 1 g liver. Increasing the supply of vitamin in the last 3 months before slaughter by 4 times (up to approximately 1000 IU per mink per day) increased its content in the liver to an average of 270 IU (from 130 to 520 IU, depending on the source of the vitamin) per 1 g of liver and when the dose is increased 10 times (2500-2700 IU per day) - up to 530 IU (from 460 to 600 IU).

Although animals under certain conditions tolerate large doses of vitamin A well - up to 40 thousand IU per 1 kg of live weight for 3-4 months (Helgebostad, 1955), nevertheless, prolonged oversaturation of the body with it is unsafe. It must be borne in mind that with an excess of vitamin A, the need of animals for tocopherol, B vitamins, and vitamin K increases (Terruan, 1969). If this circumstance is not taken into account, then the onset of one or another vitamin deficiency accelerates.

The phenomena of hypervitaminosis in female minks were observed when they were fed whale liver during pregnancy in an amount of 10% of the food weight. Without any clinical signs of poisoning, their fertility was reduced by 20-60%, mainly as a result of a decrease in the number of puppies in litters (Friend and Crampton, 1961).

Fur-bearing animals of the canine and mustelid families do not absorb plant carotene well. Therefore, it is necessary to give 13-carotene in oil solution 6-10 times more (ME) compared to retinol (Bassett, Harris and Wilke, 1946; Coombes, Ott and Wisnicky, 1940; Pereldik and Argutinskaya, 1960).

The international unit corresponds to 0.3 mcg (0.0003 mg) of pure vitamin A or 1.8-3 mcg (3-carotene).

Vitamin D (calciferols). It regulates the exchange of calcium and phosphorus in the body. In the absence or deficiency of this vitamin, rickets occurs in growing animals, which is expressed in various changes in the chest, spine, limbs, curvature and fractures of bones. In young animals, the bones with rickets are soft and easily subject to bending and breaking. Rickety puppies grow poorly, are lethargic, have poor appetite, often suffer from indigestion and are susceptible to infectious diseases. Among young females who had rickets, subsequently; There is a large percentage of unsuccessful whelping due to improperly formed bones.

The disease rickets in young animals is most often observed at the age of 2 to 4 months. In young animals at an older age and in animals that have finished growing, a deficiency of vitamin D and calcium in the feed causes a disease known as fibrous osteodystrophy. It is characterized by softening of the bones of the skull, their growth due to fibrous tissue, as a result of which the shape of the jaws changes, animals lose the ability to eat, become exhausted and often die.

According to Bassett, Harris and Wilke (1951), with sufficient calcium and phosphorus in the feed, the presence of 0.82 IU of vitamin D per 1 g of feed dry matter satisfied the needs of growing young animals.

The recommendations of Scandinavian researchers provide for minks a daily dose of vitamin of 100 IU per animal. In fur farms of the Soviet Union, it is customary to provide vitamin D at 100 IU per 1 kg of live weight of the animal. Modern diets, which include fish feed or fish oil, fully meet the need of minks, arctic foxes and foxes for this vitamin.

When rickets appears, you need to add a source of vitamin D to the food and check the animals’ supply of freshly crushed bone or bone meal.

The cases of rickets observed in fur farms were mainly due to the fact that the animals were not given sufficient sources of calcium and phosphorus in their feed or were given them in a poorly digestible form. To the disadvantage minerals Young animals during periods of intensive growth, as well as pregnant and lactating females, are especially sensitive.

Fish liver is richest in vitamin D. fatty fish, dairy products, irradiated yeast and special vitamin preparations.

Vitamin D is colorless crystals, soluble in oils and alcohol and insoluble in water. The vitamin is resistant to air oxygen at room temperature. It is destroyed when exposed to direct sunlight and temperatures above 125 ° C; is resistant to alkalis and is destroyed in the presence of mineral acids.

Vitamin D3 (cholecalciferol) of natural origin, obtained from the fat of fish and other animals, has the greatest activity. Vitamin D2 (ergocalciferol) is also widely used. It is obtained by irradiation of ergosterol, isolated industrially from yeast fungi.

Large doses of vitamin D can have toxic effects if taken over a long period of time. D-hypervitaminosis is accompanied by loss of appetite, vomiting, decreased body weight, indigestion, calcium deposition in many organs and tissues, and bone demineralization. Hypervitaminosis can occur when 10 thousand ME or more per 1 kg of live weight is given daily with food for 2-3 weeks.

Cereals and oilseeds, green plants and vegetables lack vitamin D.

Vitamin E (tocopherols) is important in the nutrition of many animal species. It maintains the normal state of reproductive function, the development of striated muscles, the resistance of erythrocytes to hemolysis, cellular respiration and other physiological processes.

In mink pups, vitamin E deficiency, experimentally induced on a synthetic diet, manifested itself as muscular dystrophy, fatty liver, and degenerative changes in the cardiac muscle and adipose tissue (Stowe and Whitehair, 1963).

In practical conditions, such violations are observed when animals are fed feed with a high content of unsaturated fat. Food containing rancid fat accelerates the onset of health problems.

Rapoport (1961), when feeding food with a high content of unsaturated fat from December to May, observed in arctic foxes that did not receive tocopherol supplements an increase in the number of unmarried and wasted females, and the birth of weak, non-viable puppies. A large number of covered females were left without offspring due to abortion, death and resorption of fetuses in the second half of pregnancy. The yield of puppies per female in the control groups, which received a vitamin E supplement in addition to the tested diets, was almost 2 times higher.

In males, vitamin E deficiency caused degeneration of the seminiferous tubules with impaired spermatogenesis. Their semen contained few spermatozoa, most of them were immobile or had pathological changes. The introduction of vitamin with food protected males from these disorders and preserved their sexual activity. Travis and Pilbeam (1978), by increasing the vitamin E content in mink feed from 31 to 138 mg per 1 kg of feed, reduced the mortality of newborn puppies from 8.3 to 5%. In females receiving a vitamin E supplement, the level of hemoglobin in the blood was significantly higher. The content of a-tocopherol in the blood plasma also increased.

The beneficial effects of vitamin E supplementation in high-fat diets have been attributed to the antioxidant properties of the vitamin.

Green and Banyan (1969) believe that vitamin E is related to the intestinal absorption and transport of some unsaturated fatty acids from long chain, and its positive effect on the body can be explained by the fact that it delays the absorption from the intestine of exogenous peroxides and certain fatty acids that have toxic properties.

Vitamin E deficiency causes steatitis in young minks, a disease also called “yellow fat.” The clinical and pathological picture of steatitis is described by Helgebostad (1967). The largest, rapidly growing, voracious puppies are most susceptible to the disease and most often die from it from July to September.

Those who have fallen are found to have swollen tissue, yellow-colored fat under the skin, and degenerative changes in the heart, skeletal muscles, liver, and sometimes kidneys.

Animals develop steatitis when fed diets high in unsaturated fats, such as fish oil, horse fat, and vegetable oils, especially if they are not stabilized with antioxidants (Helgebostad, 1971). Unsaturated fat inhibits the absorption of tocopherol in the digestive canal and, in addition, even in the initial stage of oxidation, inactivates it.

There is experimental evidence of the connection between vitamin E and iron metabolism in animals. Thus, Havre et al. (1973) observed in minks fed rancid fat a decrease in the level of hemoglobin in the blood and iron content in the liver. The addition of iron to such food did not restore the hemoglobin level to normal, and only with the simultaneous administration of an iron supplement and vitamin E did the iron content in the liver and the hemoglobin level remain normal.

Helgebostad (1974) showed that the introduction of iron glutamate into the food of female minks during pregnancy and lactation to prevent anemia ensured a higher yield of young animals, better growth and normalization of hemoglobin content in the blood of puppies only after adding vitamin E to the food in a dose of 5 mg per day. female Puppies from females who did not receive vitamin E grew worse and had a reduced amount of hemoglobin in the blood.

The connection between vitamin E and iron metabolism can be explained by the fact that iron restored in the body becomes a strong pro-oxidant, promoting the oxidation of unsaturated fatty acids, the formation of peroxides and hydroperoxides and the destruction of vitamin E.

According to Stowe et al. (1963), daily requirement mink in vitamin E is approximately 2.5 mg of y-tocopherol. When feeding fish with a high content of unsaturated fat, it is necessary to administer 4-6 times more vitamin E to animals (Wilton, 1958; Leoschke, 1960), that is, 10-15 mg of γ-tocopherol a per mink per day. Based on these data, per 100 kcal of feed it is required to give 2 mg of γ-tocopherol at moderate, 3 mg at medium and 5 mg at high levels of unsaturated fat in the diet. These values ​​are still used to determine the need for vitamin E for other species of animals. These and other indications about the need of animals for vitamin E should be considered as purely indicative, requiring further clarification. This is due to the fact that clinical and other signs by which vitamin E deficiency is determined are not specific to this deficiency and can be eliminated or delayed in manifestation by giving animals other substances.

A number of lesions caused in animals by vitamin E deficiency - steatitis ("yellow fat"), anemia, muscle weakness, hemorrhages in the subcutaneous tissue, hepatic necrosis - can be prevented, as observations have shown, by introducing selenium supplements into the feed. As an antioxidant, selenium can significantly replace vitamin E and thereby reduce the need for it.

The cases of sudden death in the summer of large, well-growing male minks with symptoms of muscular dystrophy and hemoglobinuria (blood in the urine) on Scandinavian farms stopped, and the animals were partially cured with large doses of tocopherol. Complete cure occurred when sodium selenite was added to the feed (Kjonsberg, 1975). Sodium selenite (Na2Se203) is introduced into the feed at a dose of 0.1 mg per 1 kg of dry weight of feed. It is recommended to give selenium and vitamin E alternately.

The difficulty of rationing vitamin E is also due to the fact that the activity of the tocopherols known to us is very different, while the tables usually show the total content of all forms of tocopherols in feed.

d-a-tocopherol has the highest biological activity. If we take its activity as 100%, then the activity of p-tocopherol will be 33%, γ-tocopherol - 5-8% and b-tocopherol - only 1% (Beckmann, 1955).

One milligram of synthetic dZ-a-tocopherol acetate is considered the international unit of vitamin E.

In terms of antisterile effect in rats, 1 mg of rfZ-a-tocopherol is equivalent to 1.1 IU and 1 mg of rf-a-tocopherol to 1.49 IU.

The effect of vitamin E on the reproductive functions of animals appears only after it is regularly introduced into the body for 2-4 weeks, depending on the dosage. Therefore, long before the onset of the rut, care should be taken to ensure sufficient inclusion of the vitamin in the animals’ diet.

Vegetable oils (seed fats) are the richest source of tocopherols. The amount of tocopherols and their ratio vary widely in different fats. It has been noticed that the more linoleic acid in fat (oil), the richer it is in tocopherols. Corn oil contains an average of 90 mg% of all tocopherols, soybean oil contains 130 mg%, and wheat germ oil contains .260 mg%. Less tocopherols in sunflower oil- 40 mg%, in hemp oil - 57 mg%, in flaxseed oil - 35 mg%, very little in coconut oil - 8 mg%.

a-tocopherol is found in all vegetable fats, in some it prevails over all other tocopherols. In wheat germ oil it makes up 60% of all tocopherols; the rest is mainly p-tocopherol. There is a lot of a-tocopherol in cottonseed oil (about 50%); the other half is γ-tocopherol. In corn oil, about 90% of tocopherols are γ-tocopherol and 10% are a-tocopherol. Soybean oil also contains a predominance of γ-tocopherol and little α-tocopherol.

Green vegetables and fruits contain much less tocopherols than vegetable fat. Animal products are also low in tocopherols. Summer cow butter and eggs are the richest in them (about 2 mg%).

The fat of most fish is relatively low in tocopherols, but in some species of fish the liver fat contains significant amounts. In cod fat, the vitamin E content ranges from 10 to 20 mg%; in the fat of lumpfish and some salmon, it reaches 50 mg or more per 100 g. However, it must be borne in mind that these data refer exclusively to fresh fat that has not been subjected to oxidation.

Below is the total content of tocopherols in other products.

Tocopherols are resistant to temperature, especially in the absence of oxygen: they can withstand heating up to 200 °C.

Vitamin E is easily destroyed in rancid fat and when exposed to ultraviolet rays. Due to fat oxidation, the vitamin content in long-stored products is much lower than in fresh ones. The preservation of vitamin E in oil and other preparations is ensured by the inclusion of antioxidants.

Vitamin K (phylloquinones). The most important physiological property of vitamin K is its participation in ensuring normal blood clotting. This vitamin, as a coenzyme, takes part in the biosynthesis of prothrombin and other substances directly related to the blood clotting process. With insufficient intake of vitamin K, newborns experience spontaneous bleeding during internal organs and under the skin. In adult animals, as well as in young animals, some time after birth, vitamin K deficiency usually does not occur, since this vitamin is synthesized in significant quantities by intestinal microbes and, in addition, is found in many feeds. The phenomenon of deficiency can occur in adult animals only with liver disease, when the flow of bile into the intestines weakens or stops completely. In the absence of bile, vitamin K contained in food is poorly absorbed and the liver, deprived of it, stops producing prothrombin and other substances required for blood clotting.

Travis, Ringer et al. (1961), adding vitamin K to semi-purified low-vitamin mink diets, found no change in blood clotting rate; this indicates that minks have almost no need to obtain vitamin K from the outside.

In female minks in which vitamin K deficiency was caused by the administration of dicumarol, a significant prolongation of blood clotting time, bleeding and abortions were observed (Kangas, Makelo, 1974).

There is reason to believe that fur-bearing animals are deficient in this vitamin under practical feeding conditions. Thus, in a number of farms, among newborn puppies of foxes and arctic foxes, a significant proportion of puppies are often found with intracranial, subcutaneous and internal hemorrhages. Such puppies are not viable, and many of them die in the first days after birth. According to observations, enriching the food of pregnant females with vitamin K gives a beneficial effect in such cases. The administration of vitamin K to females is especially useful, among which are individuals with diseased livers. Such animals are predisposed to bleeding. Vitamin K deficiency can also be caused by the use of various drugs during pregnancy that suppress the activity of bacteria in the intestines.

Vitamin K is widely distributed in foods. The richest in it are green vegetables and grass, cereals and legumes. Animal feed contains more than 20 times less of it than vegetables. In our country, vikasol is used as a vitamin K drug, produced in the form of powder, tablets and aqueous solution. In farms where females and newborn young animals are susceptible to hemorrhages, it is recommended to administer Vikasol to females before whelping, 1-2 mg per animal. The first time Vikasol is administered 10 days before whelping and the second time - 3-5 days. Vitamin K preparations in large doses are toxic: giving 6 mg of Vikasol per day per 1 kg of live weight causes dyspepsia, vomiting and increased salivation. Adding 10 mg of vikasol per day to the feed of pregnant minks caused intoxication after 7 days, accompanied by the appearance of non-viable young animals and even the death of individual females. It is best to provide pregnant females with vitamin K by feeding them light-grown greens and vegetable silage from green cabbage leaves, green tomatoes, carrot tops and root vegetables.

Vitamin K, isolated from alfalfa, is a light yellow oil with a melting point of 20°C. It is insoluble in water, but soluble in vegetable oils and resistant to moisture and air.

Vitamin Bi (thiamine) plays an important role in carbohydrate metabolism as a cocarboxylase coenzyme that oxidizes pyruvic acid. With insufficient intake of vitamin Bi, the breakdown of carbohydrates in the body stops at the stage of pyruvic acid, which, accumulating in the blood and tissues, causes dysfunction of the central nervous system and muscle activity.

Vitamin Bi is involved in nitrogen metabolism. Its deficiency leads to increased breakdown of nitrogenous substances and depletion of the body in protein substances.

With thiamine deficiency, the synthesis of fat in the animal's body from carbohydrates is also delayed.

In animals, thiamine deficiency leads to various disorders of the nervous and cardiovascular systems.

The clinical picture of thiamine deficiency in foxes was described by Ender and Helgebostad (1939, 1943) and Hodson and Smith (1942). After 3-5 weeks of feeding animals deprived of thiamine, animals experienced loss of appetite, difficulty moving, and spasms accompanied by convulsions. The body temperature of vitamin-deficient animals decreases by 1.5-2°C, and a sharp weakening of cardiac activity is noted. Animals with the first signs of vitamin deficiency can be cured by administering thiamine through a tube into the stomach and intramuscularly. If help is not provided in a timely manner, the disease progresses and the animals die within a day after the onset of spasms.

When autopsying animals that died from Bi-vitaminosis, severely hyperemic areas with minor hemorrhages are found in the brain tissue. The liver can be flabby and loose, clayey and dark red in color. The heart looks enlarged and in a significant proportion of the fallen there are hemorrhages visible to the naked eye. The stomach and intestines are empty at autopsy, but often they contain a tar-black or red-blooded mucous mass. One third of fur-bearing animals that died from vitamin deficiency are found to have a stomach ulcer.

Thiamine deficiency causes disruption of the reproductive cycle and embryonic development of animals (Ender et al., 1943).

Often, thiamine deficiency manifests itself only in digestive disorders in suckling young animals soon after their birth, despite the fact that their only food at this time is mother’s milk. Diarrhea in suckling young animals in such cases can be explained by the ingestion of toxic metabolic products with milk, which are formed in the mother’s body due to a lack of thiamine. These phenomena are eliminated by including liver or yeast in the feed.

Akimova (1969) found that female minks fed with food during the growth period (from July 14 to December 19) had little thiamine (0.01 mg per 100 kcal of metabolic energy), despite the fact that in subsequent periods of preparation for the rut and During pregnancy, they were fed a diet containing sufficient thiamine and other vitamins and produced much fewer puppies than females who were fed a diet containing sufficient thiamine during the growth period (0.1 mg of thiamine per 100 kcal of metabolizable energy). In the experimental group, for each staff female, 2.45 puppies were obtained and 2.04 puppies were placed; in the control group, which received thiamine supplements to the main diet, 4.5 puppies were registered and placed on a regular female.

The decrease in the yield of young animals in females raised on a diet with a low thiamine content was due to an increase in the percentage of emptying (33%) and a decrease in fertility (4.01 puppies versus 6 in the control).

In fur farms, thiamine deficiency was first observed in animals when they were fed raw freshwater fish or its waste. Green, Carlson and Evans (1941, 1942) were the first to establish that a disease of foxes with nervous phenomena observed in the USA and Norway (1942), which was called Chastek's paralysis, is associated with feeding raw freshwater fish to animals and can be prevented by oral or parenteral administration vitamin Bi.

Foxes have been found to become ill more quickly when fed heads and other fish scraps, and more slowly when fed muscle (fillets) of non-food fish.

Cooking eliminated the harmful effects of fresh fish. The disease Chastek's paralysis is caused by the enzyme thiaminase contained in fish, which destroys thiamine in the feed mixture. Thiaminase is found in shellfish and many types of marine fish.

Diets for fur-bearing animals are often deficient in vitamin Bi as a result of its destruction in the feed mixture by rancid fat. Feeding long-stored feed with a high fat content (fatty fish and its waste, silkworm pupa, meat and fish meal), as well as different types Oilcake can sometimes cause Vrhypovitaminosis. In these cases, puppies experience loss of appetite, unsatisfactory growth and often nervous attacks, which are eliminated by enriching the food with thiamine. Thiamine deficiency is often observed in lactating female minks. It manifests itself in the persistent refusal of females at the end of lactation to feed and their sharp weight loss. Based on available data (Ender and Helgebostad, 1943; Harris and Loosli, 1949; Leoschke and Elvehjem, 1959), the minimum requirement for vitamin B for fur-bearing animals can be taken as 0.1-0.2 mg per 100 g of dry matter of feed.

Since the need for vitamins varies depending on the condition of the animals, in practical conditions it is advisable to administer more than the indicated minimum amounts of thiamine to animals with food: 0.2-0.4 mg for every 100 g of dry food, that is, 50-100 mcg for every 100 kcal stern.

With a high content of carbohydrates in the feed, animals need more thiamine than with a high amount of fat.

The richest source of thiamine should be considered brewer's yeast, cereal germ. There is a relatively high amount of thiamine in the liver, kidneys and heart of farm animals. Meat, fish and offal can serve as a satisfactory source of vitamin Bi.

Synthetic preparations of vitamin Bi - thiamine chloride and thiamine bromide - are highly soluble in water and have low toxicity. In a dose exceeding the body's need by 200-300 times, they do not yet cause a toxic effect.

Thiamine is very stable in an acidic environment and easily loses activity in the presence of alkalis. At high temperature it is destroyed.

Vitamin losses during normal short-term cooking of foods amount to up to 30%. Canning of meat and fish feed

sodium pyrosulfite destroys vitamin B6. It does not change under the influence of light and oxygen in the air.

Vitamin B 2 (riboflavin) is an integral part of the yellow enzyme involved in the redox reactions of the body. Its role in carbohydrate metabolism is mainly that it, together with thiamine and nicotinic acid, oxidizes lactic acid into pyruvic acid, and the latter into carbon dioxide and water. In the absence of riboflavin or any other of these vitamins, the process of carbohydrate metabolism is disrupted and animals get sick.

Riboflavin is necessary for protein metabolism and, above all, for the proper absorption and synthesis of amino acids, since with its participation their oxidative deamidation is carried out.

The connection of riboflavin with fat metabolism is evident from the fact that an increase in the supply of fat causes an increase in the animals' need for riboflavin by 2 times or more than under normal nutritional conditions. Feeding diets high in fat and low in riboflavin has a negative effect on animal growth.

The first work related to identifying the need for riboflavin in foxes was a study by Schafer et al. (1947). On a diet without riboflavin, fox puppies began to stunt after 2 weeks, and after 3 weeks they developed muscle weakness, clonic spasms, and became comatose.

In vitamin-deficient animals, hair depigmentation and darkening of the eye lens were observed.

Additional data on the need of animals for riboflavin were obtained in their experiments by Rimeslatten (1957, 1959). When fed on a diet containing (%): fish meal from cod heads 20, oatmeal 4.5, wheat flour 9, lard 2.5, fish oil 0.5, water 63.5, with the addition of vitamins E to the feed, K, a mixture of B vitamins, with the exception of riboflavin, dermatitis, depigmentation and hair loss, muscle weakness and lens opacity were found in young blue foxes after 5-7 weeks. The author of the study, based on his observations, believes that blue fox puppies should be given at least 0.1 mg of riboflavin per 100 kcal, or 0.36 mg per 100 g of food dry matter, after weaning. The requirement of pregnant and lactating female Arctic foxes is at least 0.15 mg of riboflavin per 100 kcal. To be more confident, Rimeslatten recommends giving 0.4 mg of riboflavin per 100 kcal of feed during pregnancy and lactation and 0.25 mg of riboflavin per 100 kcal of feed for young animals. The need for riboflavin in young minks was studied by Leoschke (1960). The growth retardation of mink puppies on a purified diet without riboflavin was eliminated by adding this vitamin at 0.15 mg per 100 g of dry food.

In the experiment of Akimova (1969), young mink were raised from July 14 to December 19 on a diet of meat by-products (heads, ears 48.2%), barley flour (12.1%). stearic fat (39.7% in calorie content), supplemented with all vitamins, with the exception of riboflavin, gave a low yield of puppies the following year - almost half as much as in the control, where the same diet was supplemented with riboflavin during the growth period at the rate of 0.25 mg per 100 kcal of metabolic energy. In the experimental group, 4.2 puppies were obtained per whelping and 2.3 puppies per female taken for the experiment, and in the control, 6 and 4.5 puppies were obtained, respectively. Since December 20, both the experimental and control groups were fed a household diet containing all vitamins, including riboflavin, in sufficient quantities.

Akimova obtained similar results when feeding young minks during the growth period on a diet consisting of boiled pollock, wheat crackers and stearic fat. The exclusion of riboflavin from the mixture of B vitamins led to a decrease in the final weight of females (as of November 1) and a sharp deterioration in their reproductive abilities: for an experimental female who did not receive vitamin mixture riboflavin, 3.07 puppies were reared, and in the control group with the same feeding, but with the addition of vitamin B 2 - 6.11 puppies.

Available experimental data and practical observations indicate that riboflavin deficiency can most often occur in animals when fed diets with a moderate protein content, especially if it is represented by fish and meat waste, with a high intake of fat. Pregnant and lactating females need more vitamin than during the resting period. One of the signs of hypovitaminosis B2 may be the discovery of congenital deformities in some of the offspring: a cut palate, shortening of the bones of the limbs and abnormal skeletal development. In dark-colored animals, the hair is often bleached, especially in newborn young animals.

In all animals, including fur-bearing animals, with ariboflavinosis, the body's resistance to infections caused by pneumococci, staphylococci and salmonella decreases. In minks, this most often manifests itself in the occurrence of abscesses in the head and neck area. B2-avitaminosis is characterized by the preservation of appetite by animals until they experience profound functional disorders of various systems.

Animals are not able to accumulate significant reserves of the vitamin in their bodies. If there is a deficiency of the vitamin, its amount in all organs is reduced to one third of the norm. The liver, kidneys, heart have the highest B2 content, and there is a lot of it in other organs and tissues. For the minimum requirement of animals for riboflavin, you can take 0.1 mg per 100 kcal. During periods of growth and reproduction, it should be given at least 0.25 mg per 100 kcal.

Of the feedstuffs, the richest in riboflavin are feed and brewer's yeast, milk, liver, heart, kidneys, and muscle meat. Fish feeds and meat by-products, as well as grains, contain little riboflavin, but when fed in large quantities, the minimum requirement can be met.

Freezing products for storage and heat treatment does not lead to significant losses of the vitamin. Riboflavin is easily destroyed in an alkaline environment and in a dissolved state in the light.

The crystalline preparation of the vitamin is orange-yellow, odorless, tastes bitter, and is poorly soluble in water (10-13 mg per 100 ml of water at 27.5 ° C). In a normal saline solution, when heated to a boil, the concentration of the vitamin can be brought to 1 mg per 1 ml.

Riboflavin is low-toxic in doses several times higher than recommended. Oral administration of 10 g of the vitamin to rats and 2 g per 1 kg of live weight to dogs did not cause toxic effects.

Niacin (nicotinic acid, nicotinamide, PP) participates in numerous enzymatic reactions, catalyzing a number of processes associated with the metabolism of carbohydrates, fats, amino acids and protein.

Animals are able to synthesize nicotinic acid from tryptophan and thereby partially satisfy their need for the vitamin. However, this process is ineffective and requires 60 mg of tryptophan to form 1 mg of niacin.

Niacin deficiency, induced experimentally on synthetic purified diets, was described by Hodson and Loosli (1942) in adult foxes and by Schafer, Whitehair and Elvehjem (1947) in fox pups. Symptoms are similar to human pellagra and a canine disease known as black tongue. Vitamin deficient animals experience loss of appetite, diffuse inflammation of the gums, inner surfaces of the lips, cheeks and areas under the tongue. The mucous membranes of the mouth are easily exfoliated and emit a foul odor. Saliva can be copious, thick and sticky. The tip and edges of the tongue appear red at first, followed by dark blue lines. Animals often vomit and have debilitating bloody diarrhea. The mucous membrane of the entire gastrointestinal tract is usually inflamed. Further deprivation of niacin in foxes leads to an exacerbation of all these symptoms, complete refusal of food and water by the animals, and death. The observed unsteady gait, nervous seizures and paralysis indicated a disorder in the activity of the nervous system in vitamin-deficient animals.

In mink, niacin deficiency was experimentally induced by Warner et al. (1968). On a synthetic diet without nicotinic acid, mink puppies taken into the experiment at different ages lost their appetite, their live weight decreased, they became weaker, fell into a coma and died after 10 days. Some puppies passed blood in their feces and suffered paresis of the hind limbs.

In this experiment, tryptophan was added to a diet devoid of niacin; it was shown that minks were unable to satisfy their need for the vitamin with this amino acid.

The fact that minks need high amounts of the vitamin is evidenced by the high content of niacin in their milk compared to the milk of other animals. In 100 g of mink milk, Jorgensen (1960) found 16 mg of niacin, which is approximately 20 times the niacin content in cow's milk and 2 times more content in pig milk.

In practical conditions, with the existing type of feeding, the diets used with meat, fish and grain feeds fully satisfy the animals’ need for niacin and there is no need to worry about adding it to the feed.

Niacin deficiency can occur in animals as a complication of their pathological condition as a result of general underfeeding and disruption of digestive processes.

For various gastrointestinal diseases, especially when they become protracted, nicotinic acid can have a normalizing effect on the secretory, acid-forming and motor functions of the stomach, stimulate the enzymatic activity of the pancreas and speed up the recovery of animals.

Nicotinic acid has a positive effect in liver diseases, especially when its glycoregulatory and antitoxic functions are impaired. Since excessive niacin supplementation promotes fatty liver disease, it is recommended that sufficient sources of choline or methionine be administered simultaneously with food to prevent this. The animals' need for niacin is about 1.5 mg per 100 g of dry matter of feed, or 0.5 mg per 100 kcal.

Nicotinic acid compounds are low toxic. Toxic effects cause doses that exceed therapeutic doses by at least 1000 times.

Nicotinic acid - crystalline powder white, odorless, non-hygroscopic and very stable in dry condition to external conditions. It dissolves well in water (1 g per 60 ml) and in ethyl alcohol (1 g per 80 ml). In boiling water its solubility increases. Does not collapse when autoclaving for 20 minutes at 120 °C. Resistant to light, air oxygen, acids and alkalis.

Yeast, liver, lean meat, and legumes are rich in niacin. Satisfactory sources of niacin are whole grain flours of wheat, barley and rye. Although milk, eggs, meat and fish products are low in niacin, due to their high tryptophan content they play an important role in the prevention and treatment of vitamin deficiency.

Pantothenic acid. The main physiological significance of pantothenic acid is that it is a component of coenzyme A, which plays an important role in interstitial metabolism. Pantothenic acid is involved in the synthesis of acetoacetic and citric acids, fatty acid metabolism and many reduction and carboxylation reactions. Many aspects of protein, carbohydrate and fat metabolism are associated with pantothenic acid. Pantothenic acid is necessary to maintain normal activity of the adrenal cortex and the synthesis of adrenocorticotropic hormone. Pantothenic acid is needed by all types of animals, only a few are able to synthesize it in the body.

The symptoms of pantothenic acid deficiency in silver-black fox puppies were expressed in growth retardation, changes in hair color and increased mortality of puppies. In the dead animals, noticeable degeneration of the liver, a catarrhal state of the stomach and upper part of the small intestines and hemorrhagic changes in the kidneys - in the cortex and medulla were found; in some animals an increase in the thymus gland was noted. Vitamin deficiency was caused by feeding fox puppies from 80 days of age on diets in which fishmeal predominated, other foods were given in boiled form, and yeast was absent. The addition of pantothenic acid to this diet eliminated the above signs of deficiency. The animals did not show a deficiency of the vitamin when they began to be fed diets with fishmeal from the age of 5 months, that is, when growth basically stopped (Pereldik, 1950).

Schafer et al. (1947) observed growth retardation in fox puppies fed a synthetic diet without the addition of pantothenic acid after only 2-3 weeks. The addition of 0.25 mg of calcium pantothenate per 100 g of feed gave only a temporary improvement, while 1.5 mg completely restored the growth of animals.

Pantothenic acid deficiency in 13-week-old standard minks on a synthetic diet of casein, sucrose, lard, cottonseed oil, supplemented with amino acids, mineral salts and a mixture of vitamins, which did not contain pantothenic acid, was described in detail by McCarthy, Travis et al. (1966). During 57 days of experimental feeding, 50% of the animals died, with a final weight 2 times less than the initial one. Pantothenic acid deficiency manifested itself only in nonspecific symptoms: decreased food consumption and weight loss, exhaustion and dehydration of the body, and changes in stool consistency. At autopsy, severe emaciation and a complete absence of fat in the body, the presence of ulcers and hemorrhages in the stomach and intestines were observed.

The minimum requirement of minks for pantothenic acid for growth, according to McCarthy et al. (1966), is 0.5-0.8 mg per animal.

The need of animals for pantothenic acid for reproduction has not been studied. There are only observations (Pereldik, 1950) that adding it to the economic diets of minks and sables reduced embryonic mortality and increased the yield of puppies per female.

Vitamin deficiency can occur in fur farms when feeding animals with dry and boiled animal feed, with prolonged use of feed with rancid fat and a small supply of yeast and liver. The need for the vitamin increases with increasing fat content in the feed.

Pantothenic acid is thermolabile and is destroyed by acids and bases. It is highly soluble in water and has low toxicity.

The richest foods in pantothenic acid are yeast, liver, heart, and kidneys.

Vitamin B6 (pyridoxine) participates in enzyme processes that catalyze the reactions of transamination, deamination, and decarboxylation of amino acids in the body, having a great influence on the body’s absorption of dietary nitrogen. It also relates to the body's use of unsaturated fatty acids.

Schafer et al. (1947) caused pyridoxine deficiency in silver fox puppies on a synthetic diet lacking this vitamin. It manifested itself in weight loss and the development of anemia. Adding pyridoxine to the diet at a rate of 2 mg per 100 g of feed prevented these deficiency phenomena.

Pyridoxine deficiency in minks, caused by feeding a synthetic diet without vitamin B6 for 2 weeks, manifested itself in decreased appetite, indigestion, growth retardation and nervous phenomena - ataxia, restlessness, convulsions, apathy (Bowman, Travis, Warner, etc., 1968). Some animals have abundant discharge from the eyes, swelling of the face and nose, and symmetrical dermatitis - acrodynia.

At autopsy, dead minks were found to have fatty infiltration of the liver and kidneys, an enlarged spleen, and severe blood filling of the lungs.

Makarova (1976), having caused experimental vitamin B6 deficiency in mink puppies by introducing an antivitamin into the food - isonicotinyl hydrazide (tubazide), observed a deterioration in appetite and stunted growth of puppies already in the 2-3rd week after the start of the experiment.

After a 2-month administration of tubazide, the animals responded weakly to the distribution of food and became easily excitable and aggressive. In the sixth month of the experiment, the animals completely lost their appetite, lost weight and died in a state of deep coma. A decrease in hair density was noted in minks deprived of the vitamin. Giving minks with pronounced clinical signs of vitamin deficiency pyridoxine 3 mg per animal per day restored appetite and sharply improved the general condition of the animals.

Vitamin B6 deficiency can cause reproductive dysfunction. Thus, the addition of 8-12 mg of deoxypyridoxine, a vitamin B6 antagonist, to the daily diet of minks caused 100% infertility in pregnant females due to the death and resorption of fetuses at an early stage of their development, and in males - azospermia and degeneration of the germinal tissue of the testes (Helgebostad, Svenkerud and Ender , 1963). According to these authors, feeding minks from December 18 until whelping a feed mixture consisting (% by weight): boiled fish (saithe) -80, skimmed milk powder - 2.6, whole wheat - 11.2, beef lard - 3 ,1, groundnut oil - 2.6, sugar - 2.6 and a mixture of all vitamins, from which vitamin B6 was excluded, led to an increase in the number of empty females and, as a result, a decrease in the yield of young animals by 1.1-2.5 puppies per experimental female compared to control females who received an additional 0.6 mg of pyridoxine chloride on April 3 and 1.2 mg of vitamin from April 3 until whelping.

Rimeslatten (1963) also showed that with a lack of vitamin B6 in the feed, the number of wasted female minks increases and the yield of young animals decreases.

Large doses of pyridoxine (1.8 and 2.4 mg per 100 g dry matter) had no effect compared with daily doses of 0.9 mg (Jorgensen, 1965).

Based on the results of these experiments, it can be assumed that 0.25 mg of pyridoxine per 100 kcal meets the vitamin needs of minks at average protein levels in the diet.

A positive effect of vitamin B6 on the fertility of minks was obtained by Baalsrud and Kveseth (1965) when added to a feed mixture consisting of fish waste (45%), slaughterhouse waste (12%), blood (6%), skim milk (5%), fat (1%), carbohydrates (6%), fish oil (0.5%), vitamin supplements (5%) and water (19%), 2.5 mg of pyridoxine chloride per 1 kg of the finished mixture from February 23 to June 15. The study authors obtained a statistically significant increase in fertility. The average yield of puppies per coated female in the group with vitamin B6 supplementation (971 females) was 4.04 on May 20, and in the group without vitamin supplementation (921 females) - 3.74 puppies.

In the experiment of Makarova (1977), females who received an antivitamin in addition to a balanced diet from January 4 had a significant decrease in fertility by 0.98 puppies. The yield of puppies per main female was 1.26 fewer puppies compared to control females that received sufficient vitamin B6 in the food.

Makarova also found that in a diet containing 0.1 mg of pyridoxine per 100 kcal and without the addition of an antivitamin, young minks felt a lack of vitamin. As a result, he was stunted and had a skin of lower quality.

A deficiency of pyridoxine in the feed was indicated by a decrease in the daily excretion of 4-pyridoxylic acid in the urine in minks and the detection of xanthurenic acid in the urine when tryptophan was added to the feed.

The additional introduction of pyridoxine into this diet in an amount of 0.2 mg per 100 kcal eliminated these signs of deficiency and ensured normal growth of puppies and good hair development.

The experiments of Baalsrud and Makarova are of interest in that they indicate the possibility of pyridoxine deficiency in pregnant mink females and pups when feeding under production conditions.

Pyridoxine chloride is highly soluble in water and alcohol, insoluble in ether and chloroform, easily crystallizes, odorless, bitter in taste and almost non-toxic. It is resistant to temperature even in acid or alkali solutions and is destroyed when stored in light.

Vitamin B 12 (cyanocobalamin). The main physiological significance of vitamin B 12 is to maintain normal hematopoiesis. Insufficient intake of it into the body leads to anemia associated with impaired hematopoietic functions of the bone marrow. Cyanocobalamin takes part in a number of metabolic processes in the body. It stimulates the processes of methylation (synthesis of methyl groups) and isomerization of methyl maloic acid. These reactions are essential for the metabolism of amino acids and volatile fatty acids.

Vitamin B 12 plays a significant role in the reproduction processes of many animals. With its deficiency, reproductive capacity disorders and the birth of non-viable offspring are observed.

Fur-bearing animals, like other mammals with a simple stomach, need a constant supply of vitamin B 12 with food. Intestinal bacteria that synthesize cyanocobalamin are unable to satisfy the need of these animals for the vitamin. This was shown by Schafer et al. (1948) on foxes and by Leoschke, Labor and Elvehjem (1953) on minks. The deficiency was expressed in loss of appetite, weight loss and severe fatty degeneration of the liver. In some cases, anemia was not observed in foxes.

There is little experimental data on the effect of vitamin B 12 supplements on the growth and productivity of animals when fed with regular feed. There are observations that female minks, which were fed diets without muscle meat, fish and liver, but with a predominance of meat by-products in the animal feed group, responded positively to vitamin B 12 supplements during pregnancy. With its introduction, the number of stillborn puppies was reduced and their mortality rate in the first days of life was reduced, as a result, the yield of young animals per female increased on average by 0.8-1.2 puppies compared to the control.

It is noted that the growth effect of the vitamin is better manifested in early age and when it is administered in combination with antibiotics, which, by inhibiting the microflora, protect part of the vitamin from being absorbed by intestinal microorganisms.

The effect on increasing the viability and growth of the offspring is more pronounced when the vitamin is added to diets with a moderate content of meat and fish feed and with a predominance of offal in the animal feed group. Minks and other animals on diets in which fish feed makes up 40-50% of the weight of all animal feed are fully provided with the vitamin and do not require additional administration.

In practical feeding conditions, vitamin B 12 can have a positive effect on the condition of animals with various liver diseases, dystrophy and stunting of young animals, and chronic gastrointestinal diseases. In animals with a diseased liver, the addition of cyanocobalamin helps to normalize the basic functions of the liver, increases its antitoxic and glycogen-fixing ability and shortens the duration of the disease.

Vitamin B 12 deficiency can often occur in animals with chronic digestive disorders. In such sick animals, the mucoid cells of the fundic glands of the stomach cease to secrete mucoprotein, which is necessary for the absorption of the vitamin. This gastro-mucoprotein, known as “Kestl intrinsic factor”, is of a glucoprotein nature, usually combines with vitamin B 12 into a protein-vitamin complex and thereby protects it from absorption by intestinal bacteria. With gastritis, the secretion of gastromucoprotein stops and due to the fact that B 12 is captured by the intestinal microflora, its deficiency may occur.

Cyanocobalamin is much less absorbed by animals with pyridoxine or iron deficiency. This explains the beneficial effect of the complex use of ferrous iron preparations with vitamin B 12 on the condition of animals in which anemia is caused by insufficient intake of iron into the body.

The daily requirement of mink for vitamin B 12 is approximately 3 mcg (Leoschke, I960). This amount should be considered as the minimum required by the animal to prevent vitamin deficiency. In practical conditions, we consider it more reliable to proceed from the requirement of 5 mcg of cyanocobalamin per 1 kg of live weight. Therapeutic dose is 10-15 mcg of cyanocobalamin per 1 kg of live weight when administered parenterally 1-2 days before improvement occurs. Vitamin B 12 is non-toxic and does not cause hypervitaminosis if administered in excess.

Cyanocobalamin is a dark red crystalline powder, highly soluble in water and alcohols. At pH 4-5, it tolerates autoclaving at 100 °C. The dark red color of its crystals is due to cobalt, which is part of the vitamin molecule. In dry form, the vitamin is resistant to temperature conditions, but in solution it quickly loses activity under the influence of light.

The foods richest in vitamin B12 include the meat of cattle, horses and marine animals, the liver of farm animals and fish (especially cod), cottage cheese and milk.

Data on the content of vitamin B 12 in feed vary greatly among different authors, which is apparently due to the methods of its determination. Even if we are guided by the lower values ​​of the vitamin content that are given in the literature, then it is enough for minks to give 7-10 g of beef liver or 20-25 g of pork liver per day. A daily supply of 80-100 g of horse meat contains the amount of vitamin necessary for minks. In fish feed, the content of vitamin B 12, according to Scandinavian researchers, ranges from 1 to 10 mcg per 100 g of feed, depending on the type of fish. Fish meal contains 30-50 mcg per 100 g. There is little vitamin B 12 in cereals - about 0.1 mcg per 100 g.

Vitamin B 12 preparations are available in the form of tablets for administration and in the form of sterile solutions for injection. For the needs of livestock farming, biomass is produced from propionic acid bacteria with a relatively high vitamin content, usually indicated on certificates.

Folic acid (pteroylmonoglutamic acid), like vitamin B12, plays the role of an antianemic factor. With its deficiency, hematopoietic processes are disrupted, in particular, the formation of red blood cells, granulocytes and platelets is inhibited and leukopenia develops.

Folic acid is involved in the biosynthesis and metabolism of nucleic acids, the formation of methionine from hemocysteine. It is also needed for the synthesis of methyl groups and therefore exhibits a choline-sparing effect.

The intestinal microflora in fur-bearing animals, as in other animal species, synthesizes a significant amount of folic acid: excretion in feces exceeds its intake from food by 4-6 times. Folic acid deficiency most often occurs with the use of sulfonamides, antibiotics and other drugs that block the endogenous synthesis of the vitamin in the intestines.

In mink and foxes, folic acid deficiency was caused by feeding synthetic diets lacking folic acid to adults for 19–24 weeks and young animals for 7–14 weeks (Schafer et al., 1946, 1947; Whifehair et al., 1949 ). The young animals lost their appetite, became anemic, had loose feces with blood, and their live weight decreased. There was a significant decrease in hemoglobin and leukocytes in the blood. Hemorrhagic gastroenteritis was found in dead vitamin-deficient minks.

Adding folic acid to food at a rate of 25 mcg or more per 100 g of food led to rapid recovery of fox puppies and improved growth. For minks, the therapeutic dose turned out to be 50 mcg per animal per day; Lower doses have not been tested.

There are reports in the literature that even in commercial conditions among young minks, puppies with macrocytic and megaloblastic anemia are found, which can be cured by the administration of folic acid (Whitehair et al., 1949).

For anemia of this kind, the best therapeutic effect is achieved by combining folic acid with vitamin B 12. Folic acid is also used for some pathological conditions of the liver, since this acid has a lipotropic effect, has a beneficial effect on the level of blood phospholipids and improves bile excretion.

In feed, folic acid is in bound form. It acquires its activity in the liver under the influence ascorbic acid, when converted into folinic acid, or cytorum factor.

The need of animals for folic acid has not been established. In case of anemia or liver disease, it is recommended to give it 0.2-0.3 mg to mink and twice as much to arctic fox and fox per day until recovery. Folic acid has slight toxicity. The maximum permissible single dose is 2 mg per 1 kg of live weight. The richest foods in folic acid are yeast, liver, cauliflower, green leaves, soybeans. The crystalline preparation of folic acid is poorly soluble in water and completely insoluble in alcohol and ether. Therefore, soda solutions of the vitamin are often used. When boiled and exposed to light, it is destroyed.

Biotin (vitamin H). The physiological significance of biotin is still poorly understood. The role of the vitamin in the life of animals is associated with its possible participation in carbohydrate, fat and purine metabolism.

Domestic animals and fur-bearing animals under economic conditions, with the exception of certain cases, do not need to obtain the biotype from the outside, since it is widely distributed in feed and is synthesized in the body in significant quantities by intestinal bacteria.

Biotin deficiency in fur-bearing animals can be caused by long-term introduction into their food. large quantity raw egg whites or feeding synthetic food devoid of vitamins. Raw egg white contains albumin, called avidin, which binds the biotype in the intestine, forming an avidin-biotin complex that is not broken down by intestinal enzymes, and thus turns it off from metabolism.

Vitamin deficiency can occur more quickly in animals if, simultaneously with raw egg whites, sulfonamide drugs or antibiotics are administered to them, which inhibit the vital activity of intestinal bacteria that synthesize biotin.

A description of biotin deficiency experimentally induced in minks by feeding egg whites was given by Helgebostad et al. (1959). It manifests itself in disruption of molting and regrowth of winter hair, depigmentation, hair loss on the back and sides. Skin examination revealed thickening of the epidermis and follicular degeneration. The earlier in relation to September 15, biotin in the feed was removed from metabolism, the greater the changes in the skin and hair of the minks. The inclusion of egg white in the feed after this period does not cause significant changes in the structure and color of the hair.

In vitamin-deficient minks, cases of “self-cutting” (biting off the tops of the hair), thickening of the tip of the tail, sucking and gnawing on the tail to the point of wounds were observed. These phenomena disappeared after the minks were given biotin.

Female minks fed biotin-deficient food for up to a year became pregnant, but did not produce offspring. When minks began to be fed such food from the second half of pregnancy, they gave birth to puppies with swollen paws and gray sparse pubescence, most of which died in the first days after birth due to the fact that the females did not take care of them.

In minks lacking biotin, the liver is greatly enlarged, gray-yellow in color, and has a high fat content.

Biotin deficiency was induced by Travis et al. (1968) in minks on a purified experimental diet that did not contain avidin. This indicates that the synthesis of biotin in the intestinal tract of minks, characterized by a high rate of food passage, is not intense enough to fully satisfy the body’s need for the vitamin.

In practical conditions of fur farms, biotin deficiency can occur after prolonged feeding of animals with long-stored fatty foods. Oxidized fat from fish, sea animals, and horse meat destroys the vitamin in the feed mixture and suppresses its synthesis by the intestinal microflora.

With the by-products obtained from the slaughter of turkeys, a significant amount of egg white gets into the feed of animals with ovaries, which often causes abnormal hair development (Leoschke, 1969). Since egg white avidin loses its ability to bind biotin when heated, it is recommended to cook eggs and turkey by-products before feeding or feed them raw, but be sure to periodically exclude them from the diet.

Biotin is found in all foods of animal and plant origin. Most of it was found in yeast, liver and kidneys (180-250 mcg per 100 g); in meat and fish there is much less of it (4-8 mcg per 100 g). There is more of it in whole cereal grains (9-12 mcg per 100 g) than in whole grains (1-2 mcg). When cooking foods, about 25% of the vitamin is destroyed.

Biotin salts are highly soluble in water and alcohol. Its aqueous solutions (pH from 4 to 9) are stable at 100°C. When dry, it is resistant to heat and light. Not particularly toxic, but this needs clarification.

Choline. The physiological significance of choline is determined by its lipotropic effect. It, among other lipotropic factors, protects the liver from fatty infiltration and helps remove excess fat from the liver with such a disorder. The lipotropic effect of choline is associated with the metabolism of phospholipids: it promotes the breakdown of neutral fat in the liver and the formation of phospholipids released to nourish body tissues. Phospholipids are removed from the liver very actively, and thereby the amount of fat in it is reduced.

The accumulation of fat in the liver, caused by a lack of choline, leads to the development of necrosis with subsequent proliferation of connective tissue and causes a number of functional disorders in its activity.

The consequence of choline deficiency may be hemorrhagic renal degeneration; they increase in size, acquire a dark red color, and histological examination reveals vascular hyperemia and hemorrhages in the cortex.

Choline in the animal's body is synthesized from the essential sulfur-containing amino acid methionine and partly from betaine. Therefore, choline deficiency is more often observed when animals are fed low-value proteins with low methionine content. The animal's body is not able to fully satisfy its need for choline through biosynthesis and needs to obtain some amount of it with food.

The effect of choline in the body depends to some extent on other vitamins. Adding thiamine to a diet low in choline accelerates the onset of fatty liver disease. Nicotinic acid also causes an increase in the amount of fat in the liver if it is added to a diet with a low protein content. On the other hand, folic acid and vitamin B[2 reduce the need for choline, that is, they have a choline-sparing effect.

In fur farming practice, they resort to introducing choline into animal feed when there is a death among them with symptoms of cirrhosis and fatty infiltration of the liver. The inclusion of choline in the food of minks with fatty liver disease caused by feeding cake affected by a toxic fungus (Aspergillus niger) led to the removal of excess fat from the liver, the accumulation of glycogen in it and a noticeable improvement in the general condition of the animals. In control animals that did not receive choline supplements, their health deteriorated and they died (Pereldik, Titova, Akulova, Kuznetsova, 1965). There are observations of the same beneficial effect of giving choline to foxes and arctic foxes with fatty liver degeneration. The positive effect of cholim is more clearly manifested when the diet is simultaneously enriched with protein feeds rich in methionine (cottage cheese, muscle meat) and a reduction in fat content.

The need of animals for choline has not been established. By analogy with other animals, in particular dogs, it is recommended to give animals with food for prevention from 20 to 40 mg of choline chloride per 1 kg of live weight, for treatment - 50-70 mg, or 1% of the dry matter of the feed.

The feasibility of such additives of choline chloride to the food of minks in order to protect them from fatty liver degeneration was shown by Juokslahti et al. (1978), comparing the activity of enzymes in the blood serum of minks fed on a diet with and without the addition of choline chloride. Adding 60 mg of choline chloride per animal per day to the household diet during the breeding season significantly reduced the levels of aspartate aminotransferase, lactate hydrogenase and bilirubin in the blood serum, which serves as an indicator of improved liver function. The study authors recommend giving pregnant female minks 40 mg of choline chloride per day.

The richest source of choline is egg yolk. There is a lot of it in the liver, brain, yeast, soy flour. Meat, fish, and cereal grains are satisfactory sources of choline.

Choline chloride is a colorless crystalline powder that is highly hygroscopic. It is soluble in water and alcohols. Weak solutions of choline are thermostable.

Vitamin C (ascorbic acid) has a comprehensive effect on metabolic processes in the body. It participates in the formation of collagen, which is part of the main intermediate substance of the vascular endothelium and connective tissue, stimulates the oxidative processes occurring in the body, controls individual phases of protein metabolism, in particular the metabolism of tyrosine and phenylalanine, affects the glycoregulatory and antitoxic functions of the liver, etc.

With the exception of primates and guinea pigs, all higher animals, including fur-bearing animals, have the ability to synthesize vitamin C in their bodies. Feeding foxes, arctic foxes and minks food lacking vitamin C did not cause disease (Mathiesen, 1939). Nevertheless, cases have been established where the administration of ascorbic acid to fur-bearing animals has a beneficial effect on the health and increased viability of young animals.

In practical observations and a number of studies (Pereldik, 1950; Gusev, 1950; Afanasyev, 1961, etc.) it was noted that the introduction of vitamin C into the mouth of newborn fox puppies that had bleeding paws at birth led to an improvement in the condition of more than 70% of the young and its preservation, while 80% of puppies with the same signs of “red feet”, but not receiving vitamin C, died in the first 4-5 days after birth. Red-footed puppies were found to have a low level of vitamin C in their organs, the presence of hemorrhages in the skin, subcutaneous tissue, skeletal muscles, joint capsules, impaired formation of bone tissue and the formation of red blood cells.

Since redfoot is most often in large sizes was found in farms where foxes and arctic foxes were given little vitamin A, thiamine and B vitamins in their food during pregnancy, it was suggested that insufficient A- and B-vitamin nutrition inhibits the synthesis of vitamin C in the body of females and thereby causes poor health in puppies . The increase in the number of sick puppies when females were fed long-stored fatty foods during pregnancy was explained by the fact that rancid fats destroy the vitamins in the feed mixture.

38% of foxes that did not receive vitamin A developed characteristic symptoms of vitamin A deficiency. However, the animals did not get sick when vitamin C was added to this diet (Bassett, Loosli and Wilke, 1948).

The beneficial effect of ascorbic acid in preventing the loss of young animals with “red feet” is explained in the light of studies that have shown the protective effect of this vitamin on the state of the body in case of deficiency of vitamins B, pantothenic acid, biotin, vitamin E, etc. The addition of ascorbic acid prevents or delays the occurrence of vitamin deficiencies in deficiency of these vitamins (Terrouan, 1969). These works at the same time emphasize important the use of ascorbic acid in fur farms to eliminate possible feeding errors during such critical periods as pregnancy and lactation.

The role of ascorbic acid in animal nutrition is increasing due to its ability to effectively prevent the oxidation of fats and the appearance of peroxides harmful to the body. Vitamin C as an antioxidant can replace a significant part of the tocopherol required by animals. As a factor that has a pronounced effect on the antitoxic and glycoregulatory function of the liver, vitamin C is recommended for use in various liver diseases in animals.

Newborn fox and arctic fox puppies who develop thickening and redness of their paws on the first day of life are injected with a pipette through the mouth with a 3-5% solution of ascorbic acid, 1 ml 2 times a day until the swelling disappears. After the solution is administered, weak puppies are placed under the female and they are helped to take the nipple. It is recommended that females with sick puppies be kept in a warm room for 2-3 days. Adult females during pregnancy, as well as animals unfavorable for liver disease, should be given ascorbic acid from 10 to 20 mg per 100 kcal of food.

Ascorbic acid - white crystalline powder sour taste, highly soluble in water and alcohol and insoluble in fats. In the dark and at room temperature, ascorbic acid powder remains active for several years. Daylight and ultraviolet rays have a noticeable destructive effect on ascorbic acid - it becomes inactive. Aqueous solutions of the vitamin are especially unstable to light. Therefore they must be used on the day of preparation. Ascorbic acid is easily oxidized in an alkaline environment in the presence of even traces of metal salts - copper, silver, iron, etc. Vitamin C is non-toxic. Its excess burns in the tissues and is partially excreted in the urine.

Of the feeds, the fruits richest in ascorbic acid are rose hips, currants and other fruits. berry plants, vegetables. There is little of it in animal products and almost none in grains. It is contained (mg per 100 g): in dry rosehip pulp - 1500, in black currant - 300, in red pepper - 250, sea buckthorn - 120, in cauliflower -70, in green onions - 60, in rowan, spinach, tomatoes - 50, in fresh white cabbage, dark green salad, rutabaga - 30, in red beets, potatoes, fresh onions - 10, in muscle meat and milk - 10.

As a result of summing up the above considerations about the significance of the practical use of certain vitamin preparations in fur farming, the following conclusions arise.

Animals receiving in their diet raw sea fish, meat by-products, fishmeal (or krill) in a ratio of 1:1:1 for digestible protein and yeast (feed, brewer's, baker's) -1.5-2 g based on dry weight per 100 kcal are provided by vitamins A and D from fish, vitamin B 12 from fish, fish meal and meat by-products and many B vitamins from yeast.

It is advisable to supplement such diets with insurance supplements of vitamins E and B1 in summer and autumn and vitamins E, K, B1B2, B6, B12 and C in winter and spring. The need to enrich food with vitamin preparations in winter is mainly due to the fact that during this important period of preparing animals for reproduction, they consume relatively little food and have an increased need for vitamins. The need to add vitamin Bi is due to the fact that there is little of it in fodder and baker's yeast.

In the fur farming of the Soviet Union, multivitamin preparations are used to supplement feed with vitamins: pushnovit-1 and pushnovit-2. Both drugs are intended mainly for enriching diets with raw meat and fish feeds with B vitamins.

These preparations contain vitamins in the following quantities per 1 g of air-dry mass.

The composition of the preparations is designed so that 1 g provides the daily requirement of a mink, and 2 g of the preparation provides the daily requirement of foxes and arctic foxes for vitamins.

Pushnovit-1 is intended for animals of the main herd and Pushnovit-2 for young animals in the summer-autumn period.

Diets with a predominance of meat by-products, krill, meat and bone or fish meal, long-stored fish in the group of animal feeds, it is advisable to enrich them with vitamins A in a dose of 500 IU, D - 100 IU, E - 5 mg per animal in addition to the vitamins introduced with furnace. day.

Requirement for minerals

About 40 mineral substances are found in the animal body; Most of them do not play a role in metabolism and pass into the body with the constituent substances of the feed. Essential minerals are considered to be those that act as structural components, act as enzyme activators, or participate in cellular metabolism.

The need of animals for calcium and phosphorus. These substances are found in all tissues of the body, but the vast majority of them are found in bones (calcium 99%) - Calcium is necessary as a structural substance of supporting tissue, is involved in regulating the excitability of the nervous system, in blood clotting and in other physiological processes.

Phosphorus in the body of animals is closely related to calcium, and about 80% of the total amount is concentrated in bones and teeth. It is also found in proteins, nucleic acids and phospholipids. Phosphorus plays an important role in carbohydrate metabolism.

If there is a lack of calcium and phosphorus or each of them separately in young animals, bone formation is disrupted and a disease called rickets occurs. In adult animals, a deficiency of these substances leads to osteomalacia, a disease in which the bones become weak and brittle. With rickets, tubular bones and ribs become deformed, joints thicken and young animals grow poorly. Calcium and phosphorus deficiency negatively affects the milk production of females, the development of puppies during the milk period, and childbirth in females can be difficult and unsuccessful.

Studies of the effects of different levels of calcium and phosphorus and vitamin D on bone formation in minks have shown that the ratio of calcium to phosphorus in the diet is important. The best effect is achieved by the ratio of calcium and phosphorus in the range of 1:1 - 1.7:1. With this ratio of these minerals and a content of 0.82 IU of vitamin D per 1 g of dry matter, 0.3% calcium to the dry matter of the feed was sufficient and the same amount of phosphorus for normal bone development and good fur in young minks (Bassett, Harris and Wilke, 1951). In practical conditions, these authors recommend feeding calcium and phosphorus in an amount of 0.4% of the dry matter of the feed. Argutinskaya (1954), who studied the need of minks for these elements, came to similar conclusions. She found that young minks require calcium in the amount of 0.5-0.6% and phosphorus 0.4-0.5% of the dry matter of the feed. These cottages provide not only normal growth, but also a fairly high deposition of minerals in the body. The need of lactating female minks, according to Argutinskaya, is 0.8% calcium and 0.55% phosphorus to the dry matter of the diet. Based on the fact that in the diets used for animals, 100 kcal is equivalent to 30 g of dry matter, we can assume that the need of young minks for calcium is 0.15-0.18 g and phosphorus 0.12-0.15 g per 100 kcal. The need of a lactating female can be taken equal to 0.24 g of calcium and 0.17 g of phosphorus for every 100 kcal of food. For adult minks during all production periods, with the exception of lactation, and for young animals raised for fur, the recommended norm by Bassett et al. - 0.12 g of calcium per 100 kcal of feed.

Harris, Bassett and Wilke (1951), testing the effects of varying levels of calcium and phosphorus on the development of young foxes, found that for normal bone formation and good growth Hair needs to be given these minerals at least 0.6% of the dry matter of the feed. In another, earlier experiment performed on growing foxes, Harris, Bassett et al. (1945) found that on a diet containing 0.5% phosphorus and 0.2-0.4% calcium to the dry matter of the food, puppies exhibited signs of rickets. Adjusting calcium levels to 0.51% did not completely eliminate lameness in puppies.

Experiments on foxes and minks have shown that calcium deficiency with an excess of phosphorus or excess calcium in relation to phosphorus, that is, with an unbalanced ratio of these elements, rickets most quickly affects animals.

Pregnant and lactating female foxes need to be fed the same amount of calcium and phosphorus as female minks during these periods, namely about 0.8% calcium and 0.55% phosphorus of the dry matter of the diet. The minimum calcium requirement of adult foxes before the breeding season can be taken as 0.3% of dry matter, or 0.1 g per 100 kcal. The amount of phosphorus can be the same or 1.5 times less. The calcium and phosphorus standards given for foxes can also be extended to blue foxes.

Under economic conditions, the need of animals for phosphorus is fully satisfied by feeding boneless meat and fish feed. Calculations show that per 100 kcal of feed in typical diets of boneless animals contains about 0.17 g of phosphorus, that is, as much as is required by females during lactation. Thus, conventional diets only require calcium supplementation to reach the recommended ratio of these elements.

Fresh bone bone flour, tricalcium phosphate contain not only calcium, but also phosphorus, and in order for these elements to be included in the feed in normal proportions, it is necessary to give mineral supplements in slightly larger quantities than recommended. The normal ratio of calcium and phosphorus is achieved by adding 5 g of freshly crushed bone or 1.5 g of bone meal, 1.4 g of tricalcium phosphate or 0.5 g of chalk to the feed per 100 kcal. When introducing each of the first three fertilizers in the indicated sizes, the calcium content increases almost 3 times, and phosphorus 2 times compared to the requirement.

Widely used in fur farms, diets with fish, especially with bone meat by-products (minced meat from the heads and legs of farm animals, heads and paws of birds), contain calcium and phosphorus in quantities many times greater than the animals need for these substances. Thus, Nielsen (1970), having examined the composition of fresh animal feed produced by central feed kitchens in Denmark, found that it contained 8-12 times more calcium and 6-7 times more phosphorus than the minimum requirement. Leoschke (1969) points out that the diets used on farms, which include 35-40% meat and fish feed with bones (by weight of all feed), fully provide animals with calcium and phosphorus.

Farm rations with 6% ash satisfy minks in calcium and phosphorus (20% of ash is calcium). For lactating females, Leoschke considers it necessary to have 7% ash in the feed.

Calcium phosphate salts deserve preference among fertilizers, since they are better absorbed, easily alkalize urine and do not sharply change the ratio of calcium to phosphorus.

The need of animals for sodium and chlorine. Sodium and chlorine, along with potassium and bicarbonate ions, play an important role in regulating osmotic pressure in body fluids. Sodium is also involved in regulating the acid-base balance. Sodium deficiency causes loss of appetite, poor protein and energy utilization, growth retardation, and impaired reproductive functions in animals. Chlorine is related to gastric secretion, being part of of hydrochloric acid and sodium chloride.

Meat and fish products, unlike most plant-based foods, contain quite a lot of sodium and chlorine. Fur animals therefore feel healthy and remain highly productive on diets without the addition of these elements. According to American researchers, lactating female minks may be deficient in these elements. The deficiency is expressed in the fact that females with large offspring lose their appetite by the end of lactation, lose weight and often die from exhaustion. The death of the animals is explained by dehydration and gastric secretion disorder. These phenomena are most often observed when feeding diets with a low content of muscle meat, blood and sea fish. Hartsough (1961) showed that the introduction of sodium chloride (table salt) into the diet of lactating females from May 15 to July 1 in an amount of 0.5% by weight of raw food with a regular supply of drinking water protects females from post-lactation exhaustion.

The need of minks for table salt in all periods, with the exception of the lactation period, is equal, according to Ahman (1969), to 0.21% of the mass of raw food and is ensured by its content in ordinary household rations (Nielsen, 1970). Large salt dachas cause poisoning of animals. Minks and blue foxes are especially sensitive to excess salt. With salt poisoning, animals are initially agitated and experience profuse salivation and often vomiting. The minks then become comatose and die from suffocation. At autopsy, those who died from salt poisoning reveal hyperemia of the blood vessels of the brain, lungs, kidneys and intestinal mucosa. Pinpoint hemorrhages are sometimes observed in the heart muscle and kidneys. The liver may have a flabby consistency and uneven color. With a sufficient supply of water, minks and other animals can safely tolerate excess doses of table salt (up to 4.5 g per 1 kg of live weight). In the absence of drinking water, introducing 1.8-2 g of salt per 1 kg of live weight to minks with food already leads to salt poisoning of the animals.

According to Erin (1962), who studied toxic doses of table salt, regular inclusion of it in mink food throughout the year in an amount of 0.5% by weight of raw food inhibits the sexual functions of animals, as a result of which they have a reduced yield of young animals. These deviations from the norm are not clinically manifested in anything.

Iron requirement. Iron is an integral part of all cells of a living organism, especially hemoglobin and myoglobin, and a number of oxidative enzymes. About half of all iron in the body is contained in hemoglobin and red blood cells, and about half is contained in ferritin and hemosidrin - protein compounds that act as iron storage.

Due to the fact that the bulk of iron in the body is constantly replenished as a result of the physiological breakdown of red blood cells and hemoglobin, the need for iron in healthy animals is small. It is highest in intensively growing animals, especially during the suckling period, since the iron content in milk is very low. Iron deficiency can occur in growing animals when its absorption from food in the intestines is impaired. Iron deficiency of this nature is observed under practical conditions in minks when they are fed certain types of raw fish. Many researchers (Helgebostad, Martinsons, 1958; Sfout, Oldfield and Adair, 1960; Helgebostad, 1961; Helgebostad, Gjonnes and Svenkerud, 1961; Fedorov, 1967; Kangas, 1967, etc.) have established that some fish species, mostly cod (saithe, whiting, whiting, haddock, pollock, etc.) contain substances that bind iron in the feed mixture and convert it into an indigestible form. Cooking completely eliminates, and gutting partially reduces, the iron-binding effect of fish. Mink pups fed significant amounts of one of these fish stop growing and develop a severe form of anemia. Young animals that are given these types of fish in the first months after transfer to self-feeding. Clinically, anemia manifests itself in the fact that visible mucous and hairless areas of skin on the nose and paws become pale and the amount of hemoglobin in the blood decreases. In anemic puppies, in which the percentage of hemoglobin during the period of laying and growing winter hair is below 13, the underfur becomes discolored, and as a result, the price of the skin is greatly reduced. The hair on white-fluffed skins is usually limp, inelastic, and easily wrinkles and falls off. The underfur is discolored along its entire length, and sometimes only in certain areas. Hair discoloration can affect up to half of all puppies, but with the same feeding, many may not experience it at all or only to a small extent. This is because susceptibility to anemia is partly hereditary. By culling minks that develop anemia from year to year, it is possible to increase the resistance of the herd to this disease every year and adapt it to feeding on fish.

Feeding iron-binding fish (in raw form) to pregnant and lactating females leads to negative consequences. Females lose body weight and maternal instinct, their puppies will be born small, often with indigestion, expressed in liquid mucous discharge and vomiting. Such puppies grow poorly, many of them die at an early age, and those that survive remain small.

The work of Ender and Helgebostad (1968) suggests that the iron-binding factor is trimethylamine oxide (CH)3NO-2H20, which is a constituent of fish tissue. The above cod fish contain a lot of trimethylamine oxide.

Trimethylamine oxide reacts with iron to form insoluble iron oxide hydrates (Ender, 1972).

Research by Rapoport (1972) shows that minks, when primarily fed on fish, require exogenous iron, even in the absence of fish containing an iron-binding factor in the diet. According to him, in fish of most species the iron content is extremely low - from 0.05 to 0.1%, that is, 30-50 times less than in meat feed. The introduction of iron salts into the fish diet has a positive effect on both the yield of puppies and their condition. The addition of iron to fish diets during pregnancy increased the yield of puppies in Arctic foxes by 1.5 puppies and in minks by 0.4 puppies per female.

It is administered to animals in the feed in the form of preparations of divalent or trivalent iron in such a way that there is 2-3 mg per mink per day. It is recommended to give ferrous sulfate to pregnant females 20-30 mg every other day. Since suckling puppies receive little iron from milk, for normal development they must have a certain supply at birth, which is created if pregnant females are supplied with this element. It is advisable to give mink puppies 5-7 mg of iron sulfate per day. You can feed iron 2 times a week, increasing its dose accordingly. Iron sulfate is used in the form of a 1% solution. Other ferric acid preparations also give good results, for example ferrous lactate, added in the same doses as sulfate.

In the experiments of Rapoport (1972), positive results were obtained when iron glycerophosphate was added to the feed at a dose of 50 mg per 1 kg of live weight.

It must be borne in mind that iron preparations are added to feed mixtures that do not contain fish with an iron-binding factor, since otherwise it will not be absorbed by animals. For better use, the drugs are administered to animals 2 times a week at feeding times without cod fish. Parenteral administration of organic iron compounds - ferroglucin, etc. - effectively protects against anemia.

Ender proposed a drug - iron glutamate (Hemax), which is a complex compound of ferric iron with glutamic or ribonucleic acid. The iron in this preparation does not react with trimethylamine oxide, which makes it possible to include iron glutamate in the feed mixture with fish to protect minks from anemia (Ender, Helgebostad, 1972). Ferrous glutamate is an effective antianemic agent when fed in a low pH feed mixture. Ender recommends acidifying feed by adding hydrochloric acid or organic acids - lactic or citric.

In the Soviet Union, the drug ferroanemine, an iron complex of diethylenetriaminepenta-acetic acid, disodium salt, included in the feed mixture, was tested with positive results with fish at the rate of 20 mg of iron per mink every other day.

The richest foods in iron are yeast, liver, heart, egg yolk, peas, and oatmeal.

Feeding animals with spleen in the amount of 3-8% or blood in the amount of 12-14% of the food weight prevents the occurrence of anemia in animals (Skrede, 1973). Milk and dairy products, fish feed, as well as fats and vegetables are poor in this element.

The need of animals for copper, cobalt, manganese, zinc, iodine. A number of studies have been carried out in the Soviet Union aimed at elucidating the role of microelements in the nutrition of fur-bearing animals. The effect of feeding with microelements on the growth, quality of fur and reproductive abilities of animals was studied by Titova et al. (1960) in standard minks, Berzin (1961) in standard minks and foxes, Belugina et al. (1962) in palomino minks, Berestova (1968) in minks, arctic foxes and foxes, Vasilkov (1964) in arctic foxes, Mamaeva (1967) and Bobrov (1967) in minks, Zotova (1968) in foxes, Vinogradov (1968) in pastel minks minks, Bukovskaya (1969) in young foxes, Mikhailov (1970) in minks, Samkov (1972) in foxes, Smelovsky et al. (1975) in minks.

In all of these works, the positive effect of feeding with microelements on the survival, growth of young animals, as well as on the reproductive abilities of females in different zones of the country was noted.

However, there is evidence that the diets used in fur farming do not need to be supplemented with microelements. Thus, Pereldik and Zhukova (1974), Kiiskinen, Makela (1977) did not find a positive effect on the growth, hair quality and reproductive abilities of minks of different colors by adding copper, manganese and zinc to diets with sea ​​fish. Since most studies used mixtures of microelements, the effect of some elements on the productivity and condition of animals is difficult in many cases to separate from others. Therefore, based on the results of the experiments, it is impossible to judge which mineral substances the animals were deficient in in one case or another. The issue is complicated by the fact that most authors of the studies do not fully describe the composition of diets, at least in terms of the quantitative content of the tested elements.

Despite the fact that the need of animals for trace elements is still far from being deciphered, they should be given attention, especially when problems arise in the health and reproduction of animals.

When prescribing feeding for animals, it is necessary to take into account the conditions in which the need for certain microelements is increased and cannot be satisfied with conventional feed.

Copper. The physiological significance of this element is that it is part of many enzyme systems, is necessary for the formation of hemoglobin and is needed for normal hair pigmentation. Lack of copper in the diet causes anemia, poor growth, gastrointestinal disorders and hair discoloration. Copper is widely distributed in feed, and its deficiency can only be felt in areas where the soil and water are poor in it. There is little copper in milk, and therefore, during the suckling period, young animals born with small reserves of it may suffer from a deficiency of this element.

There are observations (Panova, 1976) that in minks with hepatosis, the copper content in the liver is 19.1% lower compared to healthy animals. White fluff, one of the clinical signs of anemia, in minks is also accompanied by a decrease in the amount of copper in the liver and spleen by 2.5-3 times, respectively.

In fur farms where cases of anemia are observed in young animals, in addition to iron salts, copper sulfate is also introduced into their feed. Copper sulfate is added to the feed 10 times less than iron sulfate. It is administered in an amount of 1-1.5 mg per mink. day. Usually copper sulfate is given in dissolved form along with ferrous sulfate. For 10 parts by weight of ferrous sulfate, take one part of copper sulfate, and from this mixture make a 1% aqueous solution for introduction into the feed mixture for animals.

It must be remembered that excessive doses of copper are toxic. Feeding copper salts in excess of the need leads to the accumulation of the element in tissues, especially in the liver, and can cause chronic poisoning.

Cobalt. The importance of cobalt in the nutrition of all animals is directly related to the physiological function of vitamin B12, of which it is included. With insufficient cobalt intake from food, animals develop a severe form of anemia due to severe inhibition of bacterial synthesis of vitamin B12 in the stomach. For animals with a simple stomach, in which the possibility of producing vitamin B12 by the microflora of the gastrointestinal canal is very limited, cobalt, according to prevailing ideas about its role in the body, cannot be of significant importance. Therefore, in fur-bearing animals, the phenomena of decreased fertility, anemia and growth retardation caused by vitamin B12 deficiency should be prevented by administering the vitamin, not cobalt.

All attempts to induce cobalt deficiency in animals with simple stomachs fed vitamin B12 in their feed have failed.

Manganese is part of body tissues. With a deficiency of this element, a decrease in the activity of bone alkaline phosphatase is observed. It has been shown in laboratory animals that manganese affects their reproductive ability. With insufficient administration of this element, puberty is delayed and ovulation is delayed? steps irregularly, the cubs are born dead and non-viable. In males, a manganese-deficient diet caused degeneration of the germinal epithelium.

In conventional feedstuffs, the manganese content is sufficient to satisfy the needs of all farm animals, with the exception of poultry.

Until the need of fur-bearing animals for manganese has been studied, it is of interest to test feeding minks, foxes and arctic foxes with this element where there are disturbances in their reproduction.

Animals can be given manganese sulfate and manganese carbonate from 0.5 to 1 mg per 100 g of dry matter of feed as a supplement. This means that an adult female mink can be fed up to 0.5 mg, and a female arctic fox and fox up to 1 mg of these salts per day. Manganese fertilizer is introduced with the feed mixture in the form of a 1% aqueous solution. Every 14 days of feeding there is a 2-week break.

Excessive intake of manganese should be avoided due to the fact that it has a certain negative effect on the balance of vitamins (in particular, thiamine and riboflavin) in the body.

Zinc. It is part of the prosthetic group of the erythrocyte enzyme carbonic anhydrase. Its deficiency affects the growth of the animal and its reproductive abilities. It is generally accepted that the amount of zinc in conventional feed products significantly exceeds any probable body need for it, and therefore there is no need to provide additional nutrition to pets.

Since the influence of zinc supplements on metabolism cannot be ruled out and there are observations about the beneficial effect of zinc supplementation during the breeding season of animals, there is a need to further study the usefulness of using the element in fur farming.

Iodine is an essential component of the thyroid hormone - thyroxine. If there is insufficient intake of iodine in the body, the formation of thyroxine stops and animals become ill with the so-called goiter. Such females give birth to weak or dead cubs with very sparse hair or completely hairless. Surviving young animals with hypothyroidism remain weak and develop poorly.

The amount of iodine in grain, meat and dairy feeds is extremely small and depends on the content of the element in the soil and water. There are areas where iodine is supplied in quantities that do not cover the minimum needs of animals for it. In such places, to maintain the normal condition and productivity of animals, especially during the breeding season, it is necessary to provide iodine supplements. There are indications that in places with calcareous soil, where the water is hard (high calcium and magnesium content), iodine deficiency due to poor absorption of the element by the body occurs more quickly.

In areas where goiter is an endemic animal disease, iodine supplements should also be used in animal diets. Since the need for iodine is still unknown, it is necessary to use those doses that, under practical conditions, prevent deficiency in this element.

It is considered sufficient to administer 0.03-0.05 mg per day to mink and 0.1 mg of potassium iodide per day to foxes and arctic foxes.

Iodine supplementation should be administered to animals primarily during pregnancy. The thyroid gland has the ability to accumulate iodine, and therefore feeding can be done not daily, but every 3-5 days. It should not exceed 10 parts per million (Aulerich et al., 1978).

There is no data on the need to add other minerals, such as potassium and magnesium, to the regular diets of animals.

When using micronutrient supplements, you must remember: most of them are strong oxidizing agents and in the feed mixture can accelerate the destruction of some vitamins. Therefore, they should be introduced with food not every day, but periodically or intermittently. The main sources of vitamins (fish oil, yeast, liver, vitamin preparations) should be given in feeding without mineral supplements.

Mineral substances in food take part in the regulation of all life processes in the body, and some of them are also structural components of tissues. The bone skeleton consists of large amounts of calcium and phosphorus, and a well-nourished person has some reserves of trace elements and fat-soluble vitamins, although most of these substances are not stored in tissues. Symptoms of micronutrient deficiency appear after several days, weeks or months of eating incomplete foods, depending on the nature of the missing component. The first obvious signs of dietary insufficiency are most often biochemical changes in metabolic processes. Clinical symptoms appear much later. The smallest amount of nutritional elements that prevents obvious metabolic disorders is usually defined as the body's minimum need for these substances.

For some substances, such as calcium, the minimum requirement cannot be determined in this way, since calcium can be washed out of the bony structures of the skeleton to support the most important functions of soft tissues. No biochemical changes are detected, but the skeleton may change so that its structures become excessively soft and fragile for the load created by the weight of the body. For nutrients of this class, the minimum required amount is that which maintains a balance between the amounts of substances supplied with food and excreted from the body. This criterion is reliable only if the initial content of this component in the human body was normal and there was no unfavorable redistribution of the component between different tissues.

The absorption and use of many nutrients varies depending on the amount they enter the body and the availability of appropriate reserves in it. For example, iron is better absorbed by those individuals whose reserves are very small, and the absorption of calcium varies depending on its content in food.

Some vitamins are produced by intestinal bacteria, some of which are beneficial and others not, so the amount of vitamins determined by analyzing excrement may be higher than the amount entering the body in food, regardless of its nutritional value or tissue reserves of a given food. nutrient(such as pantothenic acid). For these and other reasons, the usual daily rations for healthy people are considered the most optimal for meeting the vitamin needs of the human body.

Individual nutrient requirements within a homogeneous population vary, and changing conditions environment introduce additional variations in the level of these needs. Thus, the recommended amount of nutrients in the daily diet should always be higher than the minimum acceptable, theoretically calculated level. Depending on the accuracy with which the minimum acceptable amount of variability of this indicator within a population group is determined, as well as the physiological significance of this substance, the recommended intake rates should have a reliable margin of safety.

Water-soluble vitamins

Requirements for some vitamins vary with energy expenditure, so larger quantities will be required with increased energy expenditure. The requirements for water-soluble vitamins in mg per 1000 kcal are: thiamine 0.5, riboflavin 0.55 and niacin 6.6. The need for vitamin B 6 increases with increasing intake of protein into the human body and amounts to 2 mg per 100 g of the latter. The consumption rate of choline could be reduced, but only if the consumption of the essential amino acid, methionine, which is a source of methyl groups, increased. All of these water-soluble vitamins can be given to healthy individuals in doses many times greater than required without any consequences; the excess will simply be excreted in the urine.

As for the indispensability of a number of water-soluble vitamins in the normal daily human diet, the opinions of scientists vary. In the USSR, certain amounts of pangamic acid (2.5 mg per day), rutin and related bioflavonoids (50 mg per day), and inositol (1.0 g per day) are recommended. In the USA, these same substances are not considered essential components in daily diets for adults.

However, some flavonoids (especially b-naphthoflavone and quercetin pentamethyl ether) are potential inducers of microsomal enzymes that eliminate the toxicity of chemical carcinogens, and these flavonoids can be considered as pharmacological agents used in contaminated atmospheres. None of these components are harmful at recommended levels of consumption or intake from regular foods.

Fat-soluble vitamins

Since fat-soluble vitamins are stored in tissues, one might think that the daily requirement for them in everyday diets is less important than the need for other vitamins. Tissue reserves of vitamin A would be enough for several weeks if the intake of this substance into the body of a well-nourished person is insufficient. Likewise, there is no urgent need to include vitamin D in the daily diet of adults just because they are not exposed to enough sunlight.

Bring sufficient amounts of non-toxic water-soluble vitamins. The norms recommended for healthy adults in the USA and USSR are given in table. 4.

They must sufficiently provide for the needs of astronauts eating normal food.

Vitamin K is synthesized in the body by intestinal bacteria, so symptoms of deficiency will be absent until absorption processes in the small intestine are disrupted or antibiotics are introduced into the body. Vitamin E stores are likely to be depleted more quickly than others, especially if the artificial cabin atmosphere has an increased partial pressure of oxygen or the daily diet is excessively rich in polyunsaturated fatty acids. Such situations present nutrients an additional requirement is to serve as nonspecific antioxidants. Therefore, the need for vitamin E depends on the amount of other biologically active antioxidant fats contained in food products (for example, BOT - butyloxytoluene, propyl gallate).

Despite the above circumstances, for greater safety, fat-soluble vitamins should be included in the daily diet of astronauts according to the norms.

In contrast water-soluble vitamins However, excessive doses of some fat-soluble vitamins should not be taken due to potential toxicity. Normal vitamin A intake should not exceed 10,000 IU. per day, although carotenoid drugs are practically harmless. With excessive intake of b-carotene, pigmentation of the skin develops. Even one case of liver damage has been described. Only in the most extreme of circumstances, where astronauts would be completely deprived of ultraviolet radiation for long periods of time, would vitamin D supplements be needed; but in this case you should not give more than 400 IU. per day. The resulting plant form of vitamin K - phylloquinone - has no toxic properties, but synthetic form This substance - menadione - is toxic to premature babies.

Although there is no data on the toxicity of menadione in adults, it would be wiser to use only the natural form of vitamin K.

Vitamin E does not show toxic effects in doses 1000 times higher than the recommended intake level; however, there is no benefit from taking higher doses of vitamin E.

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