Selenium is an essential component of glutathione peroxidase enzymes, which protect cells against peroxidation and control concentrations of intracellular proxides. Since selenium deficiency is associated with an increased incidence of arterial thrombosis, we studied the effect of selenium on in vitro interactions between platelets and endothelial cells. Platelets from normal volunteers on a diet with (PLTSe+) or without (PLTSe-) selenium supplementation and human umbilical vein endothelial cells cultured in medium alone (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 interactions between platelets and endothelial cells using ADP and arachidonic acid as agonists. We observed that: (1) selenium-dependent glutathione peroxidase enzyme activity increased in both PLTSe+ and ECSe+, being about fivefold higher in the former; (2) platelet aggregation was inhibited by Se+ cells; (3) Se+ cells released less thromboxane B(2) (PLTSe+) and more 6-keto-prostaglandin F(1alpha) (ECSe+) than Se- cells; (4) when ECSe+ were treated with acetylsalicylic acid, the inhibitory effect of selenium on platelet aggregation disappeared; (5) the concentration of nitric oxide metabolites in Se+ 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 selenium via a mechanism that is blocked by acetylsalicylic acid and is apparently unrelated to the biosynthesis of nitric oxide metabolites.
Effects of sodium selenite on in vitro interactions between platelets and endothelial cells
RICETTI, Maria Maddalena;GUIDI, Giancesare;TECCHIO, Cristina;BELLISOLA, GIUSEPPE;RIGO, Antonella;
1999-01-01
Abstract
Selenium is an essential component of glutathione peroxidase enzymes, which protect cells against peroxidation and control concentrations of intracellular proxides. Since selenium deficiency is associated with an increased incidence of arterial thrombosis, we studied the effect of selenium on in vitro interactions between platelets and endothelial cells. Platelets from normal volunteers on a diet with (PLTSe+) or without (PLTSe-) selenium supplementation and human umbilical vein endothelial cells cultured in medium alone (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 interactions between platelets and endothelial cells using ADP and arachidonic acid as agonists. We observed that: (1) selenium-dependent glutathione peroxidase enzyme activity increased in both PLTSe+ and ECSe+, being about fivefold higher in the former; (2) platelet aggregation was inhibited by Se+ cells; (3) Se+ cells released less thromboxane B(2) (PLTSe+) and more 6-keto-prostaglandin F(1alpha) (ECSe+) than Se- cells; (4) when ECSe+ were treated with acetylsalicylic acid, the inhibitory effect of selenium on platelet aggregation disappeared; (5) the concentration of nitric oxide metabolites in Se+ 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 selenium via a mechanism that is blocked by acetylsalicylic acid and is apparently unrelated to the biosynthesis of nitric oxide metabolites.
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