Increased oxidative stress and oxidative DNA damage in non-remission schizophrenia patients

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dc.authoridOrkmez, Mustafa/0000-0001-5255-0504
dc.contributor.authorCopoglu, U. Sertan
dc.contributor.authorVirit, Osman
dc.contributor.authorKokacya, M. Hanifi
dc.contributor.authorOrkmez, Mustafa
dc.contributor.authorBulbul, Feridun
dc.contributor.authorErbagci, A. Binnur
dc.contributor.authorSemiz, Murat
dc.date.accessioned2024-09-18T20:56:52Z
dc.date.available2024-09-18T20:56:52Z
dc.date.issued2015
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractIncreasing evidence shows that oxidative stress plays a role in the pathophysiology of schizophrenia. But there is not any study which examines the effects of oxidative stress on DNA in schizophrenia patients. Therefore we aimed to assess the oxidative stress levels and oxidative DNA damage in schizophrenia patients with and without symptomatic remission. A total of 64 schizophrenia patients (38 with symptomatic remission and 26 without symptomatic remission) and 80 healthy volunteers were included in the study. 8-hydroxydeoxyguanosine (8-OHdG), total oxidant status (TOS) and total antioxidant status (TAS) were measured in plasma. TOS, oxidative stress index (OSI) and 8-OHdG levels were significantly higher in non-remission schizophrenic (Non-R-Sch) patients than in the controls. TOS and OSI levels were significantly higher in remission schizophrenic (R-Sch) patients than in the controls. TAS level were significantly lower and TOS and OSI levels were significantly higher in R-Sch patients than in Non-R-Sch patients. Despite the ongoing oxidative stress in patients with both R-Sch and Non-R-Sch, oxidative DNA damage was higher in only Non-R-Sch patients compared to controls. It is suggested that oxidative stress can cause the disease via DNA damage, and oxidative stress plays a role in schizophrenia through oxidative DNA damage. (C) 2015 Elsevier Ireland Ltd. All rights reserved.en_US
dc.description.sponsorshipGaziantep University Scientific Research Projects Unit Foundation [TF.11.30]en_US
dc.description.sponsorshipThis work was supported in part by the Gaziantep University Scientific Research Projects Unit Foundation (Project no: TF.11.30). The authors declares that there is no conflict of interest.en_US
dc.identifier.doi10.1016/j.psychres.2015.07.036
dc.identifier.endpage205en_US
dc.identifier.issn0165-1781
dc.identifier.issue1-2en_US
dc.identifier.pmid26213375en_US
dc.identifier.scopus2-s2.0-84939467631en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage200en_US
dc.identifier.urihttps://doi.org/10.1016/j.psychres.2015.07.036
dc.identifier.urihttps://hdl.handle.net/20.500.12483/12141
dc.identifier.volume229en_US
dc.identifier.wosWOS:000360772600028en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Ireland Ltden_US
dc.relation.ispartofPsychiatry Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectSchizophreniaen_US
dc.subjectSymptomatic remissionen_US
dc.subjectOxidative stressen_US
dc.subjectOxidative DNA damageen_US
dc.subject8-hydroxydeoxyguanosineen_US
dc.titleIncreased oxidative stress and oxidative DNA damage in non-remission schizophrenia patientsen_US
dc.typeArticleen_US

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