Abstract
Selenium (Se) deficiency results in decreased activity of the seleno-enzyme, glutathione peroxidase (GSHPx), an intracellular scavenger of hydroperoxides which may thereby influence the activity of various enzymes of arachidonic acid (20:4) metabolism in platelets and aortic tissue from rats. In vitro studies, performed with platelets isolated by gel-filtration, demonstrated that platelets from selenium-deficient (−Se) rats aggregated to a significantly greater extent when stimulated by ADP and collagen than those from selenium-supplemented (+Se) rats. Platelets from the −Se rats also produced more thromboxane B 2 (TXB 2) when stimulated by collagen than did those from +Se rats. In aortic tissue from −Se rats, a significant depression in the generation of prostacyclin (PGI 2)-like material was demonstrated compared to the tissue from +Se rats. Type of dietary fat and age of the animals also influenced the production of PGI 2-like activity in aortas from both +Se and −Se rats. Our results suggest that an imbalance in the production of two 20:4 metabolites — proaggregatory TXA 2 and antiaggregatory PGI 2 — could occur in response to certain physiological stresses when GSHPx activity is reduced by a selenium-deficient diet.
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