Although it has been reported that vitamin E (alpha-tocopherol) can reduce
platelet adhesiveness and aggregation in vivo, the mechanism is still unkno
wn. Therefore, the aim of the present study was to determine whether incuba
tions of platelet-rich plasma (PRP) with vitamin E influence platelet adhes
ion to cultured endothelial cells. To exclude blood plasma involvement, als
o washed platelets were pretreated with alpha-tocopherol, Vitamin E (0.5-1.
0 mM) was added to PRP or washed platelets. Endothelial cells in monolayer
were incubated with thrombin-activated platelets (1 or 2 U/ml). After 1 hr
of incubation, non-adhered platelets were removed and counted. Treating of
PRP with alpha-tocopherol inhibited platelet adhesion to endothelial cell m
onolayer. This effect was dose dependent on concentrations of alpha-tocophe
rol and thrombin. In our experiments PRP was treated with alpha-tocopherol
and endothelial cell monolayer was used as test surface. These findings agr
ee with previous observations on the adhesivity of platelets to synthetic s
urfaces after dietary vitamin E in healthy volunteers. When washed platelet
s were incubated with alpha-tocopherol, no significant reduction of adhesio
n was detectable, As preincubation of washed platelets with alpha-tocophero
l does not inhibit platelet adhesion, it may be supposed that the effect of
vitamin E does not occur in a directly cellular mechanism. The data sugges
t that alpha-tocopherol may reduce platelet adhesiveness probably after inc
orporation by plasma lipoproteins. (C) 2000 Wiley-Liss, Inc.