Synthetic byproducts of tocopherol oxidation as inhibitors of platelet function.
Vitamin E and its fully oxidized form tocopherol quinone are known inhibitors of platelet aggregation. Previous results from our laboratory have shown that the quinone was approximately equal in effectiveness to vitamin E. A recent report of a far greater inhibitory activity of the quinone produced by nitric acid oxidation of vitamin E prompted this investigation. Our studies show that the unusually high inhibition of platelet aggregation, release and cyclooxygenase activity associated with nitric acid oxidized vitamin E is due to byproducts of the oxidation process and not due to tocopherol quinone. Treatment of vitamin E acetate, a substance of mild effect on aggregation and arachidonate metabolism of platelets, with nitric acid did not produce tocopherol quinone but exerted as potent an inhibition as oxidized vitamin E. We conclude that nitric acid oxidation is unsuitable for preparation of tocopherol quinone unless the latter is carefully isolated. Oxidation with permanganate proved to be an alternate method without these difficulties.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D010084:Oxidation-Reduction; D010974:Platelet Aggregation / Q000187:drug effects*; D013329:Structure-Activity Relationship; D024505:Tocopherols; D014810:Vitamin E / Q000031:analogs & derivatives* / Q000494:pharmacology*; D024502:alpha-Tocopherol / Q000031:analogs & derivatives*
D001095:Arachidonic Acids; D014810:Vitamin E; D016718:Arachidonic Acid; D024502:alpha-Tocopherol; D024505:Tocopherols