Selenium is an essential component of glutathione peroxidase enzymes, which
protect cells against peroxidation and control concentrations of intracell
ular proxides. Since selenium deficiency is associated with an increased in
cidence of arterial thrombosis, we studied the effect of selenium on in vit
ro interactions between platelets and endothelial cells. Platelets from nor
mal volunteers on a diet with (PLTSe+) or without (PLTSe-) selenium supplem
entation and human umbilical vein endothelial cells cultured in medium alon
e (ECSe-) or supplemented with Se (ECSe+) were used. The effect of in vivo
administration or in vitro supplementation of selenium on platelet function
was investigated in an aggregometry model designed for studying the intera
ctions between platelets and endothelial cells using ADP and arachidonic ac
id as agonists. We observed that: (1) selenium-dependent glutathione peroxi
dase enzyme activity increased in both PLTSe+ and ECSe+, being about fivefo
ld higher in the former; (2) platelet aggregation was inhibited by Se+ cell
s; (3) Se+ cells released less thromboxane B-2 (PLTSe+) and more 6-keto-pro
staglandin F-1 alpha (ECSe+) than Se- cells; (4) when ECSe+ were treated wi
th acetylsalicylic acid, the inhibitory effect of selenium on platelet aggr
egation disappeared; (5) the concentration of nitric oxide metabolites in S
e+ culture media did not differ from that in Se- media. We suggest that an
antithrombotic effect on the interactions between platelets and endothelial
cells can be induced by stimulating glutathione peroxidase enzymes with se
lenium via a mechanism that is blocked by acetylsalicylic acid and is appar
ently unrelated to the biosynthesis of nitric oxide metabolites.