Quantitation of Arachidonate Released during the Platelet Phosphatidylinositol Response to Thrombin
Several workers have shown that decreases in the radioactivity of phosphatidylinositol (PI) and phosphatidylcholine (PC) occur when platelets prelabeled with radioactive arachidonic acid are treated with thrombin (see Rittenhouse-Simmons and Deykin, 1981, for review). These decreases have been attributed to arachidonate release by one of two mechanisms (Fig. 1). In one mechanism, PI is hydrolyzed by a Pi-specific phospholipase C, yielding diacylglycerol and inositol phosphate. The diacylglycerol is further hydrolyzed by a lipase or lipases, releasing arachidonic acid and other fatty acids. In the other mechanism, PC is hydrolyzed by a phospholipase A2, releasing arachidonic acid and other fatty acids from the 2-position and producing lysophosphatidylcholine (LPC). There is also some evidence that arachidonic acid is made available by the action of phospholipase A2 on phospha-tidylethanolamine.
KeywordsArachidonic Acid Phosphatidic Acid Phosphatidic Acid Inositol Phosphate Heptadecanoic Acid
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- Rittenhouse-Simmons, S., and Deykin, D., 1981, Release and metabolism of arachidonate in human platelets, in: Platelets in Biology and Pathology (J. Gordon, ed.), Elsevier/North-Holland Biomedical Press, Amsterdam, pp. 349–372.Google Scholar