Dependence of arachidonic acid (AA) metabolization in human blood platelets on reduced coenzymes.
In human platelets the metabolization of AA is linked to a consumption of the reduced coenzymes NADPH and GSH which can be attributed to about 70% to the cyclooxygenase (CO) and to about 30% to the lipoxygenase (LO) pathway. In GSH depleted platelets the conversion of AA in the LO pathway to 12-HETE is strongly impaired, whereas the formation of the stable CO products from exogenous AA is not decreased, but accelerated. When platelets are deprived from GSH by oxidation to GSSG, the release of endogenous AA from phospholipids in activated platelets is inhibited.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood*; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D003958:Diamide / Q000494:pharmacology; D005978:Glutathione / Q000097:blood*; D006801:Humans; D009249:NADP / Q000097:blood*; D010084:Oxidation-Reduction
D001095:Arachidonic Acids; D003958:Diamide; D016718:Arachidonic Acid; D009249:NADP; D005978:Glutathione; D001241:Aspirin