Sare, MBozkurt, SOnuk, EOguz, MGurel, MErcan, S2024-08-042024-08-0419960952-3278https://doi.org/10.1016/S0952-3278(96)90120-9https://hdl.handle.net/11616/93046In this study, the changes of arachidonic acid metabolites after an ischemia-reperfusion (I/R) period are investigated. The cyclooxygenase and lipoxygenase metabolites were found to be significantly increased after a 45 min period of ischemia followed by 5 min of reperfusion. Prostaglandin E(2) (PGE(2))- and leukotriene C-4 (LTC(4))-like activities did not change in the ischemic period, but they both increased after reperfusion. A cyclooxygenase inhibitor indomethacin and lipoxygenase inhibitor nordehydroguaretic acid (NDGA) decreased PGE(2)- and LTC(4)-like activities, respectively, while allopurinol and superoxide dismutase (SOD) decreased both activities. According to our results, it can be assumed that free oxygen radicals are responsible for the elevation of PGE(2)- and LTC(4)-like activities and both of these arachidonic acid metabolites and free oxygen radicals are the main necrotizing agents in ischemia-reperfusion induced damage.eninfo:eu-repo/semantics/closedAccessIntestinal IschemiaFree-RadicalsIloprost Zk-36374Rat-LiverPhospholipase-A2BiosynthesisMetabolismVerapamilNecrosisOxidaseArticle556379383901421510.1016/S0952-3278(96)90120-92-s2.0-0030458297Q2WOS:A1996WA45800002N/A