Abstract
Trypsin mediates a release of arachidonic acid with resultant increase in O2 consumption (a reflection of cyclo-oxygenase activity) by whole human platelets that is similar to thrombin's effect on these cells. The trypsin and thrombin effects can be differentiated in two ways: (1) at saturating concentrations the measured effects of trypsin greatly exceed those of thrombin; (2) EGTA [ethanedioxybis(ethylamine)-NNN'N'-tera-acetate] augments the effect of thrombin but not of trypsin. Thus trypsin and thrombin probably act at different loci in the pathway that induces phospholipase activity in human platelets.
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Selected References
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