Effects of N-acetylcysteine on arginase, ornithine and nitric oxide in renal ischemia-reperfusion injury

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dc.authorwosidAydogdu, Nurettin/ABH-9224-2020
dc.contributor.authorErbas, H
dc.contributor.authorAydogdu, N
dc.contributor.authorKaymak, K
dc.date.accessioned2024-06-12T10:52:29Z
dc.date.available2024-06-12T10:52:29Z
dc.date.issued2004
dc.departmentTrakya Üniversitesien_US
dc.description13th Balkan Biochemical Biophysical Days and Meeting on Metabolic Disorders -- 2003 -- Kusadasi, TURKEYen_US
dc.description.abstractBackground: Renal ischemia-reperfusion (I/R) is a complex syndrome involving several mechanisms such as renal vasoconstrictions, extensive tubular damage and glomerular injury. N-Acetylcysteine (NAC), a potent antioxidant by itself, may serve as a precursor for glutathione synthesis. The aim of this study was to investigate the possible effects of NAC on liver and kidney tissue arginase activity, ornithine and plasma nitric oxide levels during the I/R injury of kidney. Methods: Twenty-four female Sprague-Dawley rats divided into three groups: group 1; was given saline intraperitoneally (i.p.). Saline to group 2 and NAC (300 mg kg(-1)) to group 3 were injected i.p. 30 min before induction of ischemia. Groups 2 and 3; subjected to bilateral renal ischemia (60 min) followed by reperfusion (24 h). After the reperfusion period, the rats were sacrificed and liver and kidney tissue arginase activities, ornithine and plasma nitric oxide (NO) levels were determined. Results: NAC had an increasing effect on both of liver and kidney tissue arginase activities and ornithine levels while decreasing plasma NO concentration. Conclusion: The stimulatory effect of NAC on arginase activity may result in an inhibition of the plasma NO level. Moreover, it could be possible that one of the protective mechanisms of NAC might be through the stimulation on the both liver and kidney tissue ornithine levels. (C) 2004 Elsevier Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.phrs.2004.04.005
dc.identifier.endpage527en_US
dc.identifier.issn1043-6618
dc.identifier.issue5en_US
dc.identifier.pmid15458774en_US
dc.identifier.scopus2-s2.0-5344238204en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage523en_US
dc.identifier.urihttps://doi.org/10.1016/j.phrs.2004.04.005
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18721
dc.identifier.volume50en_US
dc.identifier.wosWOS:000224442100010en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAcademic Press Ltd- Elsevier Science Ltden_US
dc.relation.ispartofPharmacological Researchen_US
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectArginaseen_US
dc.subjectIschemia-Reperfusionen_US
dc.subjectKidneyen_US
dc.subjectNitric Oxideen_US
dc.subjectOrnithineen_US
dc.subjectAcetyl Cysteineen_US
dc.subjectSynthaseen_US
dc.subjectProtectsen_US
dc.titleEffects of N-acetylcysteine on arginase, ornithine and nitric oxide in renal ischemia-reperfusion injuryen_US
dc.typeConference Objecten_US

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