The relationship between the production of thromboxane B2 and malondialdehyde by human blood platelets.

1. The formation of thromboxane B, and malondialdehyde was studied in human plateletrich plasma, in gel-filtered platelets and in bovine platelet microsomes. 2. Exogenous sodium arachidonate was converted into thromboxane B, and malondialdehyde in a concentr ation-dependent manner. Pre-incubation of platelets with aspirin inhibited the production of both thromboxane B, and malondialdehyde, although malondialdehyde could apparently be detected in the absence of thromboxane B,. 3. The aggregating agents, thrombin, collagen and the ionophore A23187 also caused production of thromboxane B, and malondialdehyde. ADP and adrenaline produced a smaller rise whilst the endoperoxide analogue U 46619 had only a slight influence on thromboxane and malondialdehyde, even though they all induced aggregation. 4. Pre-incubation of platelets with imidazole or 1-N-butylimidazole, which inhibit thromboxane synthetase, resulted in an inhibition of both thromboxane B, and malondialdehyde formation in response to collagen. 5 . The results indicate that thromboxane B, and malondialdehyde are formed in parallel, in comparable quantities. However, under the conditions used in these studies, the apparent amounts of malondialdehyde exceed those of thromboxane B,, especially in the presence of exogenous arachidonate. Thus the thiobarbiturate