The protective role of melatonin in experimental hypoxic brain damage

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dc.authoridTutunculer, Filiz/0000-0003-3710-288X
dc.contributor.authorTütüncüler, F
dc.contributor.authorEskiocak, S
dc.contributor.authorBasaran, ÜN
dc.contributor.authorEkuklu, G
dc.contributor.authorAyvaz, S
dc.contributor.authorVatansever, Ü
dc.date.accessioned2024-06-12T10:52:04Z
dc.date.available2024-06-12T10:52:04Z
dc.date.issued2005
dc.departmentTrakya Üniversitesien_US
dc.description.abstractBackground: It is known that oxygen-derived free radicals play an important role in the pathogenesis of brain injury. Melatonin is a powerful scavenger of the oxygen free radicals. In this study, the protective effect of melatonin against the damage inflicted by reactive oxygen species during brain hypoxia was investigated in newborn rats using biochemical parameters. Methods: For biochemical analyses, the levels of lipid peroxidation product (malondialdehyde ([MDA]), levels of reduced glutathione (GSH) and the activities of superoxide dismutase (SOD) and catalase (CAT) were estimated. Results: After the third day of brain hypoxia, the brain levels of MDA increased. Pretreatment of animals with melatonin abolished the rise in MDA induced by hypoxia. GSH concentration did not increase by pretreatment with melatonin. Additonally, the activities of two antioxidative enzymes (SOD and CAT) decreased after the experimental period with melatonin only preventing the change of CAT. The activity of SOD was not influenced by melatonin administration as expected. Conclusion: In this experimental study, exogenously administered melatonin effectively protected against brain injury by oxidative stress. This protective effect of melatonin may be due to its direct scavenger activity and activation of CAT. Thus, melatonin may potentially be useful in the treatment of neurodegenerative conditions that may involve free radical production, such as perinatal hypoxia.en_US
dc.identifier.doi10.1111/j.1442-200x.2005.02085.x
dc.identifier.endpage439en_US
dc.identifier.issn1328-8067
dc.identifier.issue4en_US
dc.identifier.pmid16091083en_US
dc.identifier.scopus2-s2.0-23844490295en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage434en_US
dc.identifier.urihttps://doi.org/10.1111/j.1442-200x.2005.02085.x
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18585
dc.identifier.volume47en_US
dc.identifier.wosWOS:000230888400014en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherBlackwell Publishingen_US
dc.relation.ispartofPediatrics Internationalen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAntioxidant Enzymeen_US
dc.subjectHypoxiaen_US
dc.subjectLipid Peroxidationen_US
dc.subjectMelatoninen_US
dc.subjectIschemia-Reperfusion Injuryen_US
dc.subjectFetal-Rat Brainen_US
dc.subjectLipid-Peroxidationen_US
dc.subjectOxidative Damageen_US
dc.subjectFree-Radicalsen_US
dc.subjectSuperoxide-Dismutaseen_US
dc.subjectGlutathioneen_US
dc.subjectPigletsen_US
dc.subjectSystemen_US
dc.subjectAssayen_US
dc.titleThe protective role of melatonin in experimental hypoxic brain damageen_US
dc.typeArticleen_US

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