Effects of vitamin E therapy on ethanol-induced changes in platelet aggregation, thromboxane formation, factor VIII levels and serum lipids.
A transient increase in platelet thromboxane formation has been observed in non-alcoholics during acute ethanol intoxication and in alcoholics shortly after ethanol withdrawal. Whether these effects are related to the generation of free radicals and lipid peroxidation was investigated by using vitamin E as a free radical scavenger and inhibitor of lipid peroxide formation. The results demonstrate that a high dose of vitamin E (1800 IU) taken daily by non-alcoholic men slightly (P less than 0.05) decreases aggregation-associated platelet thromboxane formation during ethanol oxidation. Likewise, vitamin E prevents the ethanol-induced increase (P less than 0.01) in factor VIII coagulant activity. These observations suggest that the enhancement of platelet thromboxane formation and factor VIII coagulant activity by acute ethanol ingestion may be related to stimulated lipid peroxidation. By contrast, similar effects of vitamin E were not found in alcoholics shortly after ethanol withdrawal suggesting other mechanisms for their platelet hyperreactivity.
D000328:Adult; D000437:Alcoholism / Q000097:blood*; D005169:Factor VIII / Q000378:metabolism*; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D013375:Substance Withdrawal Syndrome / Q000097:blood*; D013931:Thromboxanes / Q000096:biosynthesis*; D014810:Vitamin E / Q000097:blood / Q000627:therapeutic use*
D008055:Lipids; D013931:Thromboxanes; D014810:Vitamin E; D005169:Factor VIII