Biosynthesis of Thromboxane B2 and 12‐l‐Hydroxy‐5,8,10‐heptadecatrienoic Acid in Human Platelets

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Abstract
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 12OH‐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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