Protective effects of N-acetylcysteine on triamcinolone acetonide-induced lens damage in rats

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dc.authoridAyintap, Emre/0000-0002-7537-2672
dc.contributor.authorTuzcu, Esra Ayhan
dc.contributor.authorTuzcu, Kasim
dc.contributor.authorBasarslan, Fatmagul
dc.contributor.authorMotor, Sedat
dc.contributor.authorCoskun, Mesut
dc.contributor.authorKeskin, Ugurcan
dc.contributor.authorAyintap, Emre
dc.date.accessioned2024-09-18T20:08:05Z
dc.date.available2024-09-18T20:08:05Z
dc.date.issued2014
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractObjective: To examine the relationship of cataract forming effect of intravitreal triamcinolone acetonide (IVTA) injection with oxidative status and the effect of N-acetylcysteine (NAC) on these alterations. Materials and methods: Twenty-six Wistar-Albino rats were included in the study. Rats were assigned into four groups as follows: intravitreal saline injection group (controls); IVTA injection group; IVTA + intraperitoneal NAC injection group (IVTA + NAC); and intraperitoneal NAC injection group (NAC). Triamcinolone acetonide was intravitreally injected at a dose of 1 mg. NAC was intraperitoneally injected at a dose of 150 mg/g body weight. Animals were sacrificed and lens specimens were analyzed for levels of malondialdehyde (MDA) and protein carbonyl (PC) and activities of glutathione (GSH) and glutathione peroxidase (GSH-Px). Results: We found that the MDA and PC levels of lenses were increased in the IVTA group (p < 0.01). It was seen that GSH and GSH-Px in lenses were decreased in the IVTA group (p < 0.01). NAC administration significantly ameliorated these changes in the IVTA + NAC group (p<0.05). Conclusion: These results indicate that the NAC produces a protective mechanism against IVTA-induced cataract and suggest a role of oxidative stress in pathogenesis.en_US
dc.description.sponsorshipMustafa Kemal University [1202M0108]en_US
dc.description.sponsorshipThis study was supported financially by the scientific fund of Mustafa Kemal University. Project code: 1202M0108.en_US
dc.identifier.doi10.3109/15569527.2013.857679
dc.identifier.endpage298en_US
dc.identifier.issn1556-9527
dc.identifier.issn1556-9535
dc.identifier.issue4en_US
dc.identifier.pmid24641112en_US
dc.identifier.scopus2-s2.0-84912082270en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage294en_US
dc.identifier.urihttps://doi.org/10.3109/15569527.2013.857679
dc.identifier.urihttps://hdl.handle.net/20.500.12483/8619
dc.identifier.volume33en_US
dc.identifier.wosWOS:000345498400006en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofCutaneous and Ocular Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCataracten_US
dc.subjectintravitreal triamcinolone acetonide injectionen_US
dc.subjectN-acetylcysteineen_US
dc.subjectoxidative statusen_US
dc.titleProtective effects of N-acetylcysteine on triamcinolone acetonide-induced lens damage in ratsen_US
dc.typeArticleen_US

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