FAT SOLUBLE VITAMINS
Vitamin A may be of most practical importance in cattle feed. Vitamin A is essential for normal growth, reproduction, maintenance of epithelial tissues and bone development. Vitamin A does not occur, as such, in plant material; however, its precursors, carotenes or carotenoids, are present in plants. Conversion of carotenoids to retinol is variable in ruminants and is generally lower than nonruminant animals. Vitamin A deficiency results in tissue changes and is associated primarily with vision, bone development and epithelial structure and maintenance. Signs of vitamin A deficiency are most likely to occur when cattle are fed:
• high-concentrate diets;
• winter pasture or crop residues, hay grown during drought conditions;
• feeds receiving excess exposure to sunlight, air and high temperature;
• feeds which have been heavily processed or mixed with oxidizing materials, such as minerals; and
• forages, which have been stored for long periods of time.
A supplementation alone fails to reverse the vitamin A deficiency. After the animals are given zinc supplements, their serum retinol concentrations improve, suggesting that the low serum retinol concentrations are related to zinc deficiency. The association of zinc deficiency and vitamin A metabolism in ruminants is further supported by the simultaneous reduction in retinol and retinol binding protein (RBP) in zinc deficient rats, which suggests that the low plasma retinol concentrations in zinc deficiency might be caused by an impaired ability of the deficient animals to mobilize hepatic retinol because vitamin A is stored in the liver. High dietary levels of vitamin A have depressed vitamin E utilization in most animals studied. In the dairy cow, 675,000 IU of vitamin A acetate per head per day is required to significantly depress vitamin E utilization. This is approximately 10-fold greater than the highest levels currently fed to dairy cattle and therefore should not cause a practical problem.
In general, vitamin D comprises a group of closely related antirachitic compounds. There are two primary forms of vitamin D: ergocalciferol (vitamin D2), which is derived from ergosterol and cholecalciferol (vitamin D3), which is derived from the precursor 7-dehydrocholesterol and found only in animal tissues or products. Vitamin D is required for calcium and phosphorus absorption, normal bone mineralization and bone calcium mobilization. In addition, vitamin D plays a regulatory role in immune cell function. Vitamin D is absorbed in the intestinal tract in association with lipids and the presence of bile salts. Vitamin D requirement of cattle is 250 IU/kg dry diet. Ruminants do not maintain body stores of vitamin D. Because vitamin D is synthesized by ruminant animal when exposed either to sunlight or fed sun-cured forages, they rarely require vitamin D supplementation. In calves, the most clearly defined sign of vitamin D deficiency is rickets, which is caused by the bones failure to assimilate and use calcium and phosphorus normally. Accompanying evidence frequently includes decrease in calcium and inorganic phosphorus in the blood, swollen and stiff joints, anorexia, irritability, tetany and convulsions. In older animals with vitamin D deficiency, bones weaken and easily fracture. Posterior paralysis may accompany vertebral fractures.
Vitamin E occurs naturally in feedstuffs as -tocopherol. Vitamin E, which is not stored in the body in large concentrations, is found in the liver and adipose tissue. This vitamin serves several functions including a role as an inter- and intra-cellular antioxidant and in the formation of structural components of biological membranes. The vitamin E requirement for young calves is estimated to be between 60 IU/kg dry matter. Vitamin E deficiency can be precipitated by the intake of unsaturated fats. Signs of deficiency in young calves are characteristic of white-muscle disease; including general muscular dystrophy, weak leg muscles, crossover walking, impaired suckling ability caused by dystrophy of tongue muscles, heart failure, paralysis and hepatic necrosis. To prevent these deficiencies increase the amount of selenium in rations low in vitamin E.
Relatively high levels of vitamin E are required to improve animal product quality such as extending beef color, stability and minimizing off-flavors in milk due to lipid oxidation. Vitamin E supplementation during periparturient period to cows can help in reducing mastitis by potentiating the natural defense of mammary gland through increased serum á- tocopherol levels. Concerns regarding a negative effect of vitamin A on vitamin E utilization and the suitability of currently used standard activity values for vitamin E supplements for ruminants have been raised. Synthetic and naturally derived alpha-tocopherol, and their ester forms, are commonly used as vitamin E supplements. These various forms give rise to isomer differences, ester differences and formulation differences that can affect their absorption and subsequent utilization. The current research indicates that the commonly used standard activity values based on a value of 1.00 IU per mg of alpha-tocopheryl acetate are probably too low for the ruminants. The roles of isomeric forms and gastrointestinal tract absorption have not been completely resolved regarding their effects on the bioavailability of vitamin E supplements.
The term vitamin K is used to describe a group of quinone fat-soluble compounds with characteristic antihemorrhagic effects. Vitamin K is required for the synthesis of plasma clotting factors. Two major natural sources of vitamin K are the phylloquinones (vitamin K1), found in plant sources and the menaquinones (vitamin K2), and produced by bacterial flora. For ruminants, vitamin K2 is the most significant source of vitamin K, because it is synthesized in large quantities by ruminal bacteria. Vitamin K1 is abundant both in pasture and green roughages.
The only sign of deficiency to be reported in cattle is the sweet-clover disease syndrome. This results from the metabolic antagonistic action of dicomarol which occurs when an animal consumes moldy or improperly cured sweet clover hay. Consumption of dicomarol leads to prolonged blood clotting and has caused death from uncontrolled hemorrhages. Because dicoumarol passes through the placenta the fetus of pregnant animals may be affected.