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RESEARCH PRODUCT

Involvement of hydrogen and lipid peroxides in acute tobacco smoking-induced platelet hyperactivity

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Previous studies have established that cigarette smoking results in acute platelet hyperaggregability. We investigated whether changes in plasma oxidative properties could occur after smoking and whether such changes could be responsible for this enhanced platelet activity. In the present work, we report that platelets from nonsmokers become hyperactive after incubation with plasma prepared from blood of smokers obtained 10 min after smoking. This effect was not observed with presmoking plasma and could be inhibited in vitro by adding either catalase or reduced glutathione plus peroxidase to plasma or 2,6-di-tert-butyl-p-cresol (BHT) to platelets before incubation. Comparison of pre- and postsmoking plasma showed that smoking resulted in a decrease in vitamin E (18%, P < 0.01) and increases in conjugated diene (35%, P < 0.001), thiobarbituric acid-reactive substance (23%, P < 0.02), and free fatty acid (FFA, 40%, P < 0.005) plasma concentrations. The FFA fraction was peroxidized to a higher extent when extracted from postsmoking than from presmoking plasma. This peroxidized FFA fraction enhanced the thrombin-induced aggregation of platelets from nonsmokers. This increased response was inhibited either when the peroxidized FFA fractions were isolated from plasma treated with reduced glutathione and peroxidase or by pretreatment of the platelets with BHT. We conclude that the enhanced formation of lipid hydroperoxides found in postsmoking plasma seems to be responsible for the acute and marked platelet hyperactivity observed after smoking.