Possible Interaction: Anti-Inflammatory Agents, Non-Steroidal and Arachidonate

“ NSAIDs compete with the most commonly presented substrate, arachidonate , for the active site of the enzyme [3,4].”

“They are generated from arachidonate by the action of cyclooxygenase isoenzymes, and their biosynthesis is blocked by nonsteroidal antiinflammatory drugs , including those selective for inhibition of cyclooxygenase-2.”

“Inhibition of arachidonate cyclooxygenase by nonsteroidal antiinflammatory drugs reduces renal PGE2 and PGI2, exaggerates renal vasoconstriction, and thereby decreases renal blood flow and glomerular filtration rates.”

“However, certain anti-inflammatory drugs and other agents, that can interfere with the metabolism of arachidonate via lipoxygenase pathways, do significantly reduce basal PMN leukocyte-endothelial interactions.”

“ NSAIDs block the activity of both COX isozymes, COX-1 and COX-2, which mediate the enzymatic conversion of arachidonate to prostaglandin H2 (PGH2) and other prostaglandin (PG) metabolites.”

“ Non-steroidal anti-inflammatory drugs (NSAIDs) are considered to exert their activity by interfering with the generation of arachidonate metabolites in various cells, mainly in neutrophils and monocytes.”

“ Nonsteroidal anti-inflammatory drugs and sulfinpyrazone compete dose-dependently with arachidonate for binding to platelet cyclooxygenase.”

“Some non-steroid anti-inflammatory drugs which inhibit arachidonate cyclo-oxygenease have been examined for their effects on leukocyte migration, prostaglandin production and oedema formation in carrageenin-induced inflammation in the rat.”

“Several nonsteroidal anti-inflammatory drugs (NSAID) which are known to be inhibitors of collagen-induced platelet aggregation and release, as well as inhibitors of prostaglandin synthetase, are able to block the effect of arachidonate in vivo .”

“The action of non-steroidal anti-inflammatory drugs (NSAIDS) has been ascribed to their ability to block the reaction of arachidonate with cyclooxygenase/peroxidase, thus inhibiting the cellular production of inflammation mediators such as prostaglandins and leukotrienes.”