In this study, we investigated whether vitamin E at concentrations achievab
le in blood after supplementation inhibits platelet function in humans. Gel
-filtered platelets were incubated 30 minutes with scalar concentrations (5
0 to 250 mmol/L) of vitamin E and then stimulated with collagen. Compared w
ith controls, vitamin E inhibited collagen-induced platelet aggregation and
thromboxane A2 formation in a dose-dependent manner. Furthermore, vitamin
E inhibited, in a dose-dependent manner, Ca2+ mobilization and formation of
inositol 1,4,5-triphosphate, Because it was previously shown that hydrogen
peroxide formation mediates arachidonic acid metabolism and phospholipase
C activation in collagen-induced platelet activation, we investigated wheth
er vitamin E was able to blunt hydrogen peroxide. In experiments performed
in unstimulated platelets supplemented with hydrogen peroxide and in collag
en-stimulated platelets, vitamin E was able to blunt hydrogen peroxide. In
6 healthy subjects given vitamin E for 2 weeks.(600 mg/d), we found a signi
ficant decrease of collagen-induced H2O2 formation, platelet aggregation, a
nd calcium mobilization. This study demonstrated in vitro and ex vivo that
vitamin E inhibits collagen-induced platelet activation by blunting hydroge
n peroxide formation.