Erdosteine ameliorates PTZ-induced oxidative stress in mice seizure model

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dc.authoridKoçer, Abdulkadir/0000-0003-2866-555X
dc.authoridAladag, M. Arif/0000-0003-3872-3741
dc.authoridArmutcu, Ferah/0000-0002-3218-9480
dc.authorwosidKoçer, Abdulkadir/I-5287-2013
dc.authorwosidAladag, M. Arif/ABI-1182-2020
dc.authorwosidArmutcu, Ferah/A-1364-2019
dc.contributor.authorIlhan, A
dc.contributor.authorAladag, MA
dc.contributor.authorKocer, A
dc.contributor.authorBoluk, A
dc.contributor.authorGurel, A
dc.contributor.authorArmutcu, F
dc.date.accessioned2024-08-04T20:14:43Z
dc.date.available2024-08-04T20:14:43Z
dc.date.issued2005
dc.departmentİnönü Üniversitesien_US
dc.description.abstractThe role of oxygen-derived free radicals has been suggested in genesis of epilepsy and in the post seizure neuronal death. The aim of this study was to investigate whether erdosteine has a preventive effect against epilepsy and postepileptic oxidative stress. The mice (n = 27) were divided into three groups: (i) PTZ-induced-epilepsy group (it = 9); (ii) PTZ-induced-epilepsy + erdosteine group (it = 9); (iii) control group (n = 9). The animals were observed for a period of 30 min for latency to first seizure onset, total seizure duration, the number of seizure episodes. Then they were sacrificed and the brains were quickly removed, and frozen for biochemical analysis. Malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD) and xanthine oxidase (XO) activities were carried out in the brain tissue. The latent period between PTZ induction and seizure are longer in the PTZ + erdosteine group than in PTZ-induced-epilepsy group (P < 0.05). Biochemical analyses of brain tissue, revealed a significant increase in the MDA, XO and NO levels in the PTZ group according to erdosteine group. SOD level did not change in this group. While MDA and XO levels are significantly lower, SOD level is significantly higher in the PTZ + erdosteine group compared to PTZ and control groups (P < 0.01). The present study demonstrated that erdosteine treatment both may increase latent interval between seizures and may decrease oxidative stress, thus may ameliorate neuronal death in brain during seizures. It may be used as an adjunct therapy in epilepsy. (c) 2005 Elsevier Inc. All rights reserved.en_US
dc.identifier.doi10.1016/j.brainresbull.2005.02.027
dc.identifier.endpage499en_US
dc.identifier.issn0361-9230
dc.identifier.issue6en_US
dc.identifier.pmid15862921en_US
dc.identifier.scopus2-s2.0-18144413142en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage495en_US
dc.identifier.urihttps://doi.org/10.1016/j.brainresbull.2005.02.027
dc.identifier.urihttps://hdl.handle.net/11616/93903
dc.identifier.volume65en_US
dc.identifier.wosWOS:000229352300005en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherPergamon-Elsevier Science Ltden_US
dc.relation.ispartofBrain Research Bulletinen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjecterdosteineen_US
dc.subjectepilepsyen_US
dc.subjectoxidative damageen_US
dc.subjectbrainen_US
dc.titleErdosteine ameliorates PTZ-induced oxidative stress in mice seizure modelen_US
dc.typeArticleen_US

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