Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026850 (muscular dystrophy)
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This presentation reviews highlights of the first 20 years (1922-1942) of vitamin E. It begins with background information leading to identification of an antisterility factor for rats of both sexes and its acceptance into the vitamin family as vitamin E (1925). Research of the next 12 years revealed a multiplicity of deficiency manifestations: embryonic mortality, testis degeneration, encephalomalacia and exudative diathesis in the chick, and nutritional muscular dystrophy in avian and mammalian species. Toward the close of this period came the isolation of vitamin E from natural sources, determination of its empirical formula, and introduction of the designation alpha-tocopherol for vitamin E (1936). Within the next two years the structural formula of alpha-tocopherol was elucidated, its chemical synthesis accomplished, and its production from natural plant oils by molecular distillation was well established. The existence of other tocopherols with lesser degrees of biological activity became recognized. Also, the concurrent development of a chemical method for determining the vitamin E content of alpha-tocopherol in foods, body tissues and body fluids, which replaced the very laborious bioassay procedure, greatly facilitated later advances in knowledge of the distribution and nature of vitamin E.
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PMID:The first two decades of vitamin E. 32 68

The Food and Nutrition Board of the Institute of Medicine recently published a comprehensive evaluation of antioxidants in human diets that includes dietary reference intakes for vitamin E. The new dietary reference intake is 15 mg (35 mol)/d for adults, which is 50% greater than the generous allowance in the 10th edition of Recommended Dietary Allowances published in 1989. Much of the data interpreted in these publications came from studies sponsored by the Committee of Nutritional Studies at Elgin State Hospital (Elgin, IL) of an earlier Food and Nutrition BOARD: The 50% increase in the recommended dietary allowances for vitamin E is not supported by any new data. It is possible that the publication of the Institute of Medicine did not take into consideration the effects of the oxidized lipids in the diets used to promote the development of vitamin E deficiency. If lipids, oxidized to remove tocopherols, had not been a part of the experimental diets, the minimum requirement for vitamin E would have been too small for possible evaluation. Studies on the different effects of saturated and oxidized lipids in the production of encephalomalacia in chicks and muscular dystrophy in rats are reviewed. The tolerable upper intake level of vitamin E supplementation is reported to be 1000 mg/d. It is possible that the universal consumption of aspirin may not have been taken into consideration when this level was determined. Vitamin E plus aspirin may increase the tendency to hemorrhage, which makes a lower upper intake level worth consideration.
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PMID:Critique of the requirement for vitamin E. 1191 70

Production of testicular degeneration in the antioxidant-deficient rat resembles encephalomalacia in the chick in its dependence on essential (omega6) fatty acids and is distinct from the generalized response to all polyunsaturated fatty acids seen in nutritional muscular dystrophy in the rat. The nonessential (omega3) polyunsaturated fatty acids, however, lower the essential fatty acid content of the testicular lipids only slightly, are not themselves incorporated into this tissue to any appreciable degree and thus do not show the inhibitory effect on production of the antioxidant-deficiency sign noted in the studies on encephalomalacia. A direct relationship between the essential fatty acid content of the testes and the rate of testicular degeneration was found, but no effects of biologically available selenium and sulfur amino acids were evident. As the liver and muscle, onset of antioxidant-deficiency is characterized by a decrease in the most highly unsaturated fatty acid in the tissue (22ratio5-omega6 in this case) and a net increase in arachidonate.
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PMID:The effect of antioxidant deficiency on tissue lipid composition in the rat. III. Testes. 1780 34