Animal vitamins

In experimental animals, vitamin E deficiency results in resorption of femses and testicular atrophy. Dietary deficiency of vitamin E in humans is unknown, though patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic fiver disease suffer deficiency because they are unable to absorb the vitamin or transport it, exhibiting nerve and muscle membrane damage. Premamre infants are born with inadequate reserves of the vitamin. Their erythrocyte membranes are abnormally fragile as a result of peroxidation, which leads to hemolytic anemia. 

Altered vitamin A homeostasis, primarily manifested as decreased hepatic storage of vitamin A, is another established effect of PBBs in animals. Vitamin A is essential for normal growth and cell differentiation, particularly differentiation of epithelial cells, and some PBB-induced epithelial lesions resemble those produced by vitamin A deficiency. Because it is the primary storage site for vitamin A, the liver has a major role in retinol metabolism. Esterification of dietary vitamin A, hydrolysis of stored vitamin A, mobilization and release into the blood of vitamin A bound to retinol-binding protein, and much of the synthesis of retinol-binding protein occurs in the liver. 

Fat-soluble vitamins, in addition to their antioxidative effects on lipids, appear to exert a general protective effect in animals. Vitamin A and beta-carotenes protect lab animals from toxicity of citral, cyclophosphamide and some hydrocarbons (Seifter et al, (A2.) In related but independent studies, it was observed that high levels of vitamin A inhibit tumorogenesis and that low levels of vitamin A appear to enhance tumorogenesis (Baird, (1 ). vitamin E inhibited chemically-induced carcinogenesis in test systems (Shamberger, ) and also reduced the susceptibility of rats to cigarette smoke (Chow,... 

In vitro, and in experimental animals, vitamin A has anticancer action related to its role in modulating gene expression and tissue differentiation. It retards the initiation and growth of some experimental tumors. However, it only shows these effects at toxic levels, and a number of synthetic analogs. 

In experimental animals, vitamin E deficiency depresses immune system function, with reduced mitogenesis of B and T lymphocytes, reduced phagocytosis and chemotaxis, and reduced production of antibodies and interleukin-2. This suggests a signaling role in the immune system (Moriguchi and Muraga, 2000). 

Potassium dichromate and atrazine may increase the toxicity of mercury, although these effects have been noted only with metallic and inorganic mercury. Ethanol increases the toxicity of methylmercury in experimental animals. Vitamins D and E, thiol compounds, selenium, copper, and possibly zinc are antagonistic to the toxic effects of mercury. 

The effect of pectin consumption on mineral balance has not been studied extensively although the excretion and apparent balance of most minerals appears to be unaffected by dietary pectin. Iron utilization or absorption may be affected by pectin consumption but the longer feeding studies did not report any significant changes in apparent balance from control levels. Further longterm studies are needed. Interaction of pectin with vitamins has been studied little in man or animals. Vitamin C consumption with pectin may be beneficial to hypercholesterolemic persons. Vitamin... 

In animals, vitamin K2 carboxylates glutamate residues in certain proteins, to give carboxyglutamate. This modification allows the protein to bind calcium, an essential event in the blood clotting cascade. Carboxylation of glutamate residues occurs in other proteins that are active in the mobilization or transport of calcium. 

In animals, vitamin K2 carboxylates glutamate residues in certain proteins, to give y... 

The vitamin also seems to act directly on the bones, since in vitamin D deficiency more matrix is present, independent of the ash content. This contention is also supported by observations on the citric acid content, which is greatly reduced in the bones of vitamin D-deficient animals. Vitamin D administration to rachitic rats is followed by a rapid increase of the citric acid content of the bones actually preceding the increase in ash, in contrast to the very slow effect of a phosphate cure. ... 

Plastoquinols/plastoquinones and tocopherols/tocopherylquinones serve as redox systems in cell respiration and photosynthesis (E 2.2). Tocopherols and tocopherylquinones are vitamins for humans and higher animals (vitamin E, E 2.1). 2-Methyl- and 2-ethylbenzoquinone are constituents of the defense secretions of certain beetles (E 5.1). 

Most vitamins required by man are required also by all other animals. Vitamin C is an exception most animals manufacture ascorbic acid from glucose, by the following enzyme-catalyzed oxidation reactions ... 

The definition of a vitamin has been extended by some (Spector, 1980) to Include those chemical compounds required by a specific tissue but not synthesized by that tissue. For example. In certain species, vitamin C can be synthesized from glucose In the liver but not In the Central Nervous System therefore, vitamin C Is not considered a vitamin for these animals. Vitamin C for the brain must be drawn from the blood, from the vitamin C that entered the blood from the diet, or was synthesized In the liver. Subsequently, vitamin C could be considered a vitamin for the brain since It must be obtained from outside the brain. Another example Is the vitamin niacin, which cannot be synthesized from tryptophane In mammalian brain however, the synthesis of niacin from tryptophane occurs In mammalian liver (Spector and Kelly, 197.9 Spector, 1979). 

In animals vitamin Bjj is synthesized more efficiently in the gut, and ruminant animals such as cows and sheep can manufacture this vitamin for their own use. 

In pregnant animals vitamin Bi deficiency may induce resorption of the fetus. There may be prolongation of pregnancy, and there may be difficulty in bearing the young. Miscarriages are frequent. These changes are similar to those caused by simple inanition. 

Cirrhosis of the liver in man is often found in chronic alcoholism and is probably due to dietary deficiency. In active fatty alcoholic cirrhosis, choline administration has been shown to lead to a decrease in liver fat. An increase in the rate of phospholipid turnover, following administration of 10 g. of choline or methionine, has been demonstrated in patients with cirrhosis who had evidence of fatty infiltration of the liver as shown by biopsy. In animals, vitamin B12 and folic acid are intimately related to choline and methionine metabolism and are important in the prevention of fatty livers under certain conditions. Whether these vitamins are related to accumulation of fat in the liver and cirrhosis in man remains to be ascertained. The value of high protein diets in the prevention and treatment of experimental dietary cirrhosis in animals is well established there is much evidence that such is also true in man (see also p. 521). 

In experimental animals, vitamin E deficiency results in a number of different conditions ... 

It is significant that attention first became focussed on the nutrient requirements of those bacteria which are among the most exacting in this respect. This was either because the complex media they required for growth were easily injured in preparation (owing to the presence of essential labile substances) and thus rendered nutritionally deficient, or because unusual nutrient supplements were required. Thus the question of the nutrient requirements of bacteria became differentiated as a particular problem of bacteriology in much the same way as the human and animal vitamin problem forced itself on the attention of biochemists, namely as a problem of nutritional deficiency. 

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