| The 3 main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various dietary and environmental factors. |
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Encephalomalacia is seen in commercial flocks if diets are low in vitamin E, an antioxidant is either omitted or not present in sufficient quantities, or the diet contains a reasonably high level of an unstable, unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too
advanced. Encephalomalacia may or may not respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum. |
| The classical sign of encephalomalacia is ataxia, which results from hemorrhage and edema within the molecular and granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the molecular and granular layers of the cerebellar folia. Due to its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant.
The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants will prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E, or in chicks fed vitamin E-depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E are also less susceptible to lipid peroxidation in the brain. The fact that antioxidants can
help prevent encephalomalacia but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma. |
| A vitamin E deficiency accompanied by a sulfur amino acid deficiency results in a severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker’s degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results
in an increase in lysosomal enzymes, the function of which appears to be the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy showed that the addition of selenium at 1-5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E-deficient diet that was low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely
effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which by itself had no effect on the disease. |
| Studies on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have brought some order to the previous confusion about the role of vitamin E in chick nutrition. It is now apparent that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in the prevention of muscular dystrophy in the chicken. Glutathione peroxidase is soluble and is therefore located in the aqueous portions
of the cell, while vitamin E is located mainly in the hydrophobic environments of membranes and in lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in the prevention of deficiency signs. |
