Recent epidemiological studies have provided evidence supporting the potent
ial benefits of antioxidants in coronary prevention. We have investigated t
he effects of vitamin E on platelets, monocytes and endothelial cells in vi
tro. Pre-incubation of platelets with vitamin E inhibited subsequent thromb
in- (P<0.05, n=5), collagen- (P<0.0001, n=5) and ADP-(P<0.05, n = 4) induce
d platelet aggregation measured using a microtitre plate method, or convent
ional aggregometry. The adhesion of thrombin-activated platelets to collage
n was also inhibited by vitamin E (P< 0.05, n = 8), but not by vitamin C (P
>0.05, n=8); nor was the adhesion of unstimulated platelets significantly a
ffected (P> 0.05, n= 8). Pre-incubation of monocytes with vitamin E inhibit
ed their subsequent adhesion to plastic (P< 0.05, n = 9), and was also asso
ciated with an 18% reduction in adhesion to EA.hy 926 endothelial cells (n=
8), although this failed to reach statistical significance. Pre-incubation
of the endothelial cells with vitamin E also significantly reduced subsequ
ent mononuclear cell adhesion by 56% (P< 0.05, n = 3).