Protective effects of N-acetylcysteine on cyclosporine-A-induced nephrotoxicity

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dc.authorid, ahmet/0000-0001-6274-5700
dc.authoridYonden, Zafer/0000-0003-0708-5417
dc.contributor.authorDuru, Mehmet
dc.contributor.authorNacar, Ahmet
dc.contributor.authorYonden, Zafer
dc.contributor.authorKuvandik, Gfiven
dc.contributor.authorHelvaci, Mehmet Rami
dc.contributor.authorKoc, Ahmet
dc.contributor.authorAkaydin, Yesim
dc.date.accessioned2024-09-18T20:13:43Z
dc.date.available2024-09-18T20:13:43Z
dc.date.issued2008
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractObjectives. Cyclosporine A (CsA) is used for the treatment of autoimmune and inflammatory disorders. However, CsA-induced nephrotoxicity remains an important clinical problem, and oxidative stress has been implicated as a possible responsible mechanism. We assessed the protective ability of N-acetylcysteine (NAC), an antioxidant, against CsA-induced nephrotoxicity. Materials and Methods. Wistar albino rats were randomly assigned into four groups. Group I rats were treated with sodium chloride as control, group 2 with CsA, group 3 with CsA and NAC, and group 4 with NAC alone. Animals were sacrificed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), malondialdehyde (MDA) and nitric oxide (NO) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. Kidney sections were analyzed for MDA and NO levels and SOD and GSH-Px activities, as well as histopathological changes. Results. Overall, the treatment of rats with CsA alone produced significant increases in NO and MDA levels and significant decreases in SOD and GSH-Px activities in serum and renal samples. Morphological changes, including tubular epithelial atrophy, vacuolizations, and cellular desquamations, were clearly observed in the rats treated with CsA alone. Concurrent NAC administration with CsA improved renal function, as indicated by lower BUN and Cr values. Moreover, NAC significantly reduced MAD and NO levels and increased SOD and GSH-Px activities in serum and renal tissue, as well as provided a histologically proven protection against CsA-induced nephrotoxicity. Conclusion. These results indicate that NAC produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role for oxidative stress in pathogenesis.en_US
dc.identifier.doi10.1080/08860220801985942
dc.identifier.endpage459en_US
dc.identifier.issn0886-022X
dc.identifier.issn1525-6049
dc.identifier.issue4en_US
dc.identifier.pmid18569921en_US
dc.identifier.scopus2-s2.0-45749122808en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage453en_US
dc.identifier.urihttps://doi.org/10.1080/08860220801985942
dc.identifier.urihttps://hdl.handle.net/20.500.12483/9337
dc.identifier.volume30en_US
dc.identifier.wosWOS:000256352500017en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofRenal Failureen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectcyclosporine Aen_US
dc.subjectnephrotoxicityen_US
dc.subjectN-acetyleysteineen_US
dc.subjectoxidative stressen_US
dc.subjectlaboratory studyen_US
dc.titleProtective effects of N-acetylcysteine on cyclosporine-A-induced nephrotoxicityen_US
dc.typeArticleen_US

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