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Discover Supplement-Drug Interactions
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Last Updated: 5 years ago
supplement:
Arachidonate
Research Papers that Mention the Interaction
“ NSAIDs compete with the most commonly presented substrate, arachidonate , for the active site of the enzyme [3,4].”
Fatty acid ethyl ester, a non‐oxidative ethanol metabolite, reverses the inhibitory effect of ibuprofen on platelet aggregation“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.”
The effects of non-steroid anti-inflammatory drugs on leukocyte migration in carrageenin-induced inflammation.“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.”
Antioxidation theory of non-steroidal anti-inflammatory drugs based upon the inhibition of luminol-enhanced chemiluminescence from the myeloperoxidase reaction
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