Vitamin E is the principal lipid-soluble antioxidant in human plasma, and s
ome studies indicate that it may provide cardiovascular protection. To inve
stigate putative mechanisms for vitamin E in this regard, the effect of vit
amin E on vascular function and platelet aggregation was examined. In anima
l models of endothelial dysfunction, vitamin E improved the activity of end
othelium-derived nitric oxide, and this effect was not dependent upon the a
ntioxidant protection of LDL. In fact, vitamin E improved endothelial funct
ion in part due to the inhibition of protein kinase C (PKC) stimulation. Th
is activity of vitamin E was examined in platelets, and vitamin E inhibited
platelet aggregation in part through a mechanism that involves PKC, Moreov
er, the platelet inhibitory activity of vitamin E was independent of its an
tioxidant action because platelet inhibition was still observed with isofor
ms of vitamin E that were devoid of antioxidant activity.