MODULATION OF THE PLATELET THROMBOXANE A2 AND AORTIC PROSTACYCLIN SYNTHESIS BY DIETARY SELENIUM AND VITAMIN-E

Vitamin E and selenium (Se) interact synergistically as an important antioxidant defense mechanism. Se, an essential component of glutathione peroxidase (GSH-Px) and vitamin E decompose fatty acid hydroperoxides and hydrogen peroxides generated by free radical reactions. Vitamin E and GSH-Px may modulate arachidonic acid metabolism and the activity of cyclooxygenase enzymes by affecting peroxide concentration. The balance between arterial wall prostacyclin (PGI2) production and platelet thromboxane (TX)A2 directly influences platelet activity. In order to elucidate the differential role of dietary vitamin E and Se in aortic PGI2 and platelet TXA2 synthesis, 1-mo-old F344 rats were fed semipurified diets containing different levels of vitamin E (0, 30, 200 ppm) and Se (0, 0. 1, 0. 2 ppm) for 2 mo. Thromboxane B2 (TXB2) and 6-keto-PGF1-alpha, were measured by radio-immunoassay (RIA) after incubation of whole blood and aortic rings at 37-degrees-C for 10 and 30 min, respectively. Vitamin E deficiency reduced plasma vitamin E to 5-17% of control-fed rats, and supplementation increased it to 53% of the control-fed rats. Se supplementation in vitamin E-supplemented animals increased plasma GSH-Px by 17%, compared to vitamin E-deficient rats. Se and vitamin E supplementation did not have a similar effect on TXB2 and PGI2 synthesis. Se deficiency did not alter platelet TXB2 synthesis, but significantly decreased aortic PGI2 synthesis. It was necessary to supplement with both antioxidants in order to increase PGI2 synthesis. Se and vitamin E deficient groups had a higher TXB2/PGI2 ratio (0.17 +/- 0.08) compared to Se- and vitamin E-supplemented groups (0.03 +/- 0.01). These results confirm previous reports in humans and animals and are in accordance with epidemiological data indicating an inverse relationship between plasma Se and platelet aggregation. Thus, further suggesting that vitamin E and Se may have a specific role in controlling TXA2 and PGI2 synthesis.