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.

Effect of organic sulfur compounds on the chemical and enzymatic transformations of prostaglandin endoperoxide H2.

The effects of several sulfur organic compounds on the enzymatic and non-enzymatic transformations of prostaglandin endoperoxide H2 to prostaglandins were studied. Mercaptoethanol, methional alpha-lipoic acid and dimercaptopropanol increased the chemical (i.e.

Chemical and enzymatic transformations of prostaglandin endoperoxides: evidence for the predominance of the 15-hydroperoxy pathway.

Cyclic prostaglandin endoperoxides prostaglandin G2 and H2 are intermediates formed in the biosynthesis of prostaglandins from arachidonic acid. These endoperoxides can be converted chemically or enzymatically to prostaglandins E2, D2 and F2alpha. The effects of several reducing compounds on the chemical and enzymatic transformations of prostaglandins G2 and H2 were studied in order to determine the possible existence of two alternative enzymatic pathways for the conversion of prostaglandin G2 to prostaglandins.