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The effects of indomethacin, NDGA, allopurinol and superoxide dismutase on prostaglandin E2 and leukotriene C4 levels after mesenteric ischemia-reperfusion injury

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dc.contributor.author Sare, M.
dc.contributor.author Bozkurt, S.
dc.contributor.author Onuk, E.
dc.contributor.author Oguz, M.
dc.contributor.author Gurel, M.
dc.contributor.author Ercan, S.
dc.date.accessioned 2022-10-06T09:35:29Z
dc.date.available 2022-10-06T09:35:29Z
dc.date.issued 1996
dc.identifier.issn 09523278 (ISSN)
dc.identifier.uri http://hdl.handle.net/11616/62871
dc.description.abstract In 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 E2( PGE2)- and leukotriene C4 (LTC4)-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 PGE2- and LTC4-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 PGE2- and LTC4-like activities and both of these arachidonic acid metabolites and free oxygen radicals are the main necrotizing agents in ischemia-reperfusion induced damage.
dc.source Prostaglandins Leukotrienes and Essential Fatty Acids
dc.title The effects of indomethacin, NDGA, allopurinol and superoxide dismutase on prostaglandin E2 and leukotriene C4 levels after mesenteric ischemia-reperfusion injury


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