ArticlePharmaceutical research2026
Effects of Normothermic Hepatic Ischemia-Reperfusion Injury on the Hepatic Disposition of Arachidonic Acid and Its Cytochrome P450-Generated Metabolites in Rats.
Article in Pharmaceutical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeCytochrome P450 (P450) metabolites of arachidonic acid (AA) are potential therapeutic targets in ischemia-reperfusion (IR) injury, yet their disposition and actions in hepatic IR are unknown. Cellular AA and its P450 metabolites are primarily bound to lipid membranes, resulting in negligible free concentrations. This study investigates how hepatic IR injury impacts the disposition of free AA and its major P450 metabolites in rats.
methodsRats underwent 60 min of partial (70%) ischemia or sham surgery, followed by 5 min, 3 h, or 24 h of reperfusion. The effects of IR injury on free concentrations of AA and its major P450-generated metabolites in the liver were studied using LC-MS/MS. The activities of phospholipase A
resultsHepatic IR injury significantly increased free liver concentrations of AA (sevenfold) and its metabolites (1.8-9.1-fold) only in the 5-min group. Similarly, PLA
conclusionsLiver IR injury rapidly increases liver concentrations of free P450-mediated metabolites of AA, likely due to IR-induced release of preformed metabolites and AA from lipid membranes, rather than an increase in P450 enzymatic activity.
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