Enhanced malondialdehyde formation in reserpinized rabbit blood platelets

Abstract

Reserpine depressed the level of stored serotonin in rabbit platelets as low as 5% of the control 17 hours after intraperitoneal injection. The serotonin-depleted platelets produced a significantly larger amount of malondialdehyde(MDA) and aggregated more rapidly in response to thrombin as compared with the control platelets. The measurement of MDA formed from arachidonic acid by the platelet homogenates revealed no difference in cyclooxygenase activity between the serotonin-depleted and the control platelets. Reserpine added in vitro, slightly suppressed the thrombin-induced aggregation and MDA formation, and cyclooxygenase activity of the platelet homogenates. Externally added serotonin to the serotonin-depleted platelets slightly inhibited the thrombin-induced MDA formation. Serotonin, however, did not influence the cyclooxygenase. The addition of arachidonic acid to the incubation system reduced the hypersensitivity of the serotonin-depleted platelets. These results suggest that the hypersensitivity of the serotonin-depleted platelets in thrombin-induced MDA formation could be attributed to acceleration of the steps other than that catalysed by fatty acid cyclooxygenase. It is conceivable that an increased liberation of arachidonic acid from lipid or an acceleration of MDA formation from prostaglandin endoperoxide is responsible for the hypersensitivity of the reserpine-treated rabbit platelets to thrombin.