Effect of I-deprenyl and gliclazide on oxidant stress/antioxidant status and DNA damage in a diabetic rat model

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dc.contributor.authorAlper, Gülinnaz
dc.contributor.authorİrer, Seda
dc.contributor.authorDuman, Erdal
dc.contributor.authorÇağlayan, Osman
dc.contributor.authorYılmaz, Candeğer
dc.date.accessioned2020-06-25T17:40:50Z
dc.date.available2020-06-25T17:40:50Z
dc.date.issued2005
dc.departmentKırıkkale Üniversitesi
dc.description.abstractBackground: This study investigates the possible effect of monoamine oxidase inhibitor ( MAOI), selegyline ( 1-deprenyl), in combination with oral antidiabetic-gliclazide ( OAD), in preventing oxidative stress in streptozotocin-induced diabetes model in male Swiss Albino rats by measuring oxidant stress/DNA damage and antioxidant levels. Methods: Diabetic rats were divided into four groups ( n = 10) as ( 1) diabetic untreated ( DM), ( 2) deprenyl treated ( DM + D), ( 3) gliclazide treated ( DM + O), and ( 4) gliclazide and deprenyl treated ( DM + O + D). Controls were divided into two groups ( n = 8) ( 1) untreated ( C), and ( 2) deprenyl treated ( C + D). Gliclazide 5 mg/kg and/or MAOI 0.25 mg/kg daily were given orally by gavage for 4 weeks. At the end of the 12th week, catalase and superoxide dismutase ( SOD) levels in erythrocyte lysates ( EL); total antioxidant status ( TAS), 8-hydroxy-deoxyguanosine ( 8-OHdG), malondialdehyde ( MDA), and vitamin A and E levels in plasma, MDA, and MAO in liver homogenates were determined. Results: Diabetic rats showed a decrease in EL-SOD, plasma TAS, and vitamin E, and an increase in plasma 8-OHdG, plasma, and liver MDA levels ( p < 0.05). Gliclazide and/or deprenyl decreased 8OHdG levels and increased antioxidant levels and survival when compared with untreated diabetic rats ( p < 0.05). The lowest 8-OHdG levels were determined in the DM + O + D group. Conclusions: The combined treatment of deprenyl and gliclazide may contribute to the control of the physiopathological mechanisms underlying both the process of aging and type 2 diabetes by reducing oxidant stress and DNA damage, improving antioxidant status, and increasing survival, and may have implications for further clinical studies.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.1080/07435800500371805
dc.identifier.endpage212en_US
dc.identifier.issn0743-5800
dc.identifier.issn1532-4206
dc.identifier.issue3en_US
dc.identifier.pmid16392622
dc.identifier.scopus2-s2.0-28844476159
dc.identifier.scopusqualityQ3
dc.identifier.startpage199en_US
dc.identifier.urihttps://doi.org/10.1080/07435800500371805
dc.identifier.urihttps://hdl.handle.net/20.500.12587/3564
dc.identifier.volume31en_US
dc.identifier.wosWOS:000233635100005
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofEndocrine Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectdiabetes mellitusen_US
dc.subject8-OHdGen_US
dc.subject1-deprenylen_US
dc.subjectgliclazideen_US
dc.subjectoxidant stressen_US
dc.subjectantioxidant statusen_US
dc.titleEffect of I-deprenyl and gliclazide on oxidant stress/antioxidant status and DNA damage in a diabetic rat modelen_US
dc.typeArticle

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