Thrombosis |
Correspondence to Prof Pier Paolo Gazzaniga, Dipartimento di Medicina Sperimentale e Patologia, Università degli Studi di Roma "La Sapienza," Viale Regina Elena 324, 00161 Roma, Italy. E-mail gazzaniga{at}axrma.uniroma1.it
AbstractIn this study, we investigated whether vitamin E at concentrations achievable in blood after supplementation inhibits platelet function in humans. Gel-filtered platelets were incubated 30 minutes with scalar concentrations (50 to 250 mmol/L) of vitamin E and then stimulated with collagen. Compared with controls, vitamin E inhibited collagen-induced platelet aggregation and thromboxane A2 formation in a dose-dependent manner. Furthermore, vitamin E inhibited, in a dose-dependent manner, Ca2+ mobilization and formation of inositol 1,4,5-triphosphate. Because it was previously shown that hydrogen peroxide formation mediates arachidonic acid metabolism and phospholipase C activation in collagen-induced platelet activation, we investigated whether vitamin E was able to blunt hydrogen peroxide. In experiments performed in unstimulated platelets supplemented with hydrogen peroxide and in collagen-stimulated platelets, vitamin E was able to blunt hydrogen peroxide. In 6 healthy subjects given vitamin E for 2 weeks (600 mg/d), we found a significant decrease of collagen-induced H2O2 formation, platelet aggregation, and calcium mobilization. This study demonstrated in vitro and ex vivo that vitamin E inhibits collagen-induced platelet activation by blunting hydrogen peroxide formation.
Key Words: antioxidants platelet aggregation arachidonic acid metabolism phospholipase C enzyme thromboxane A2
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P. Pignatelli, F. M Pulcinelli, A. Celestini, L. Lenti, A. Ghiselli, P. P. Gazzaniga, and F. Violi The flavonoids quercetin and catechin synergistically inhibit platelet function by antagonizing the intracellular production of hydrogen peroxide Am. J. Clinical Nutrition, November 1, 2000; 72(5): 1150 - 1155. [Abstract] [Full Text] [PDF] |
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