Biosynthesis of Thromboxane B₂ and 12‐l‐Hydroxy‐5,8,10‐heptadecatrienoic Acid in Human Platelets: Evidence for a Common Enzymatic Pathway

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.