Demonstrates that thromboxane B2 and 12OH-17:3 are likely derived from a common intermediate in human platelets, providing insight into platelet biochemical pathways.
Supports shared intermediate in platelet thromboxane synthesis; leaves open in vivo human relevance and clinical translation.
Human platelet microsomes convert prostaglandin H2 to thromboxane B2 and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (12OH-17:3) in approximately equimolar amounts. The synthesizing activities of both products appear to go in parallel, both activities gradually decline upon storage and are equally destroyed by heat inactivation. Furthermore imidazole, a potent inhibitor of thromboxane synthetase activity, is an equally effective inhibitor of 12OH-17:3 formation in platelets. These results suggest that both thromboxane B2 and 120H-17:3 are derived from a common intermediate. We propose two alternative pathways for the conversion of prostaglandin H2 to thromboxane A2 and 12OH-17:3 in human platelets. The first pathway depicts thromboxane A2 as the common intermediate for the formation of both thromboxane B2 and 12OH-17:3. In the second pathway, prostaglanding H2 is converted to an activated intermediate which is converted to either thromboxane A2 or 12OH-17:3.
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Raz et al. (1978) studied this question.
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