Biological actions and possible uses of vitamin E.
Symptoms of Vitamin E deficiency can be generally attributed to derangement of processes depending upon the integrity of cellular and subcellular membranes, following the formation of tissue-damaging products of lipid peroxidation. Antioxidants modulate also the formation of products derived from long-chain polyunsaturated fatty acids, such as arachidonic acid--which are structural components of biological membranes--through oxidative reactions involving the cyclooxygenase and lipoxygenase systems. Vitamin E inhibits the aggregatory responses of blood platelets to aggregating agents "in vitro", after a preincubation period required for the uptake of the compound by the cells. The antiaggregatory activity of alpha-tocopherol, however, does not appear to be strictly dependent upon inhibition of the formation of thromboxane, the proaggregatory compound derived from arachidonic acid through be cyclooxgenase system. The effects of Vitamin E on platelet function may be of relevance in the control of thromboembolic processes of clinical importance.
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D004347:Drug Interactions; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D006801:Humans; D008054:Lipid Peroxides / Q000378:metabolism; D008954:Models, Biological; D010974:Platelet Aggregation / Q000187:drug effects; D012643:Selenium / Q000378:metabolism*; D013923:Thromboembolism / Q000517:prevention & control; D014810:Vitamin E / Q000502:physiology* / Q000627:therapeutic use; D014811:Vitamin E Deficiency / Q000378:metabolism
D000975:Antioxidants; D005231:Fatty Acids, Unsaturated; D008054:Lipid Peroxides; D014810:Vitamin E; D012643:Selenium