1. The formation of thromboxane B 2 and malondialdehyde was studied in human platelet-rich plasma, in gel-filtered platelets and in bovine platelet microsomes. 2. Exogenous sodium arachidonate was converted into thromboxane B 2 and malondialdehyde in a concentration-dependent manner. Pre-incubation of platelets with aspirin inhibited the production of both thromboxane B 2 and malondialdehyde, although malondialdehyde could apparently be detected in the absence of thromboxane B 2 . 3. The aggregating agents, thrombin, collagen and the ionophore A23187 also caused production of thromboxane B 2 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 2 and malondialdehyde formation in response to collagen. 5. The results indicate that thromboxane B 2 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 2 , especially in the presence of exogenous arachidonate. Thus the thiobarbiturate reaction used to assay malondialdehyde may detect other products of lipid peroxidation. 6. Platelet thromboxane B 2 concentrations did not always relate to the extent of aggregation. In particular, platelet aggregation could occur in the absence of detectable thromboxane B 2 production.