Considerable epidemiologic data suggest that dietary consumption of vitamin
E reduces the incidence of cardiovascular disease. The precise mechanisms
are not clear, but emerging data indicate that vitamin E has numerous activ
ities that may, in part, explain its effect on vascular disease. Ln particu
lar, vitamin E enhances the bioactivity of nitric oxide, inhibits smooth mu
scle proliferation, and limits platelet aggregation, One common mechanism t
o account for these effects of vitamin E is the inhibition of protein kinas
e C stimulation, In the setting of atherosclerosis, inhibition of protein k
inase C by vitamin E would be expected to maintain normal vascular homeosta
sis and thus reduce the clinical incidence of cardiovascular disease.