Neuroprotective effect of quercetin against oxidative damage and neuronal apoptosis caused by cadmium in hippocampus

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dc.authorscopusid7006356462
dc.authorscopusid26432848600
dc.authorscopusid24436194200
dc.authorscopusid36023238400
dc.authorwosidAktas, Cevat/D-8468-2011
dc.contributor.authorKanter, Mehmet
dc.contributor.authorÜnsal, Cüneyt
dc.contributor.authorAktaş, Cevat
dc.contributor.authorErboğa, Mustafa
dc.date.accessioned2022-05-11T14:14:01Z
dc.date.available2022-05-11T14:14:01Z
dc.date.issued2016
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Ruh Sağlığı ve Hastalıkları Ana Bilim Dalı
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalı
dc.description.abstractThe purpose of the present investigation was to evaluate cadmium (Cd)-induced neurotoxicity in hippocampal tissues and beneficial effect of quercetin (QE) against neuronal damage. A total of 30 male rats were divided into 3 groups: control, Cd-treated, and Cd + QE-treated groups. After the treatment, the animals were killed and hippocampal tissues were removed for biochemical and histopathological investigation. Cd significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in hippocampal tissue compared with the control. Administration of QE with Cd significantly decreased the levels of MDA and PC and significantly elevated the levels of antioxidant enzymes in hippocampal tissue. In the Cd-treated group, the neurons of both tissues became extensively dark and degenerated with pyknotic nuclei. The morphology of neurons in Cd + QE group was well protected, but not as neurons of the control group. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd-treated group. Treatment of QE markedly reduced the immunoreactivity of degenerating neurons. The results of the present study show that QE therapy causes morphologic improvement in neurodegeneration of hippocampus after Cd exposure in rats.
dc.identifier.doi10.1177/0748233713504810
dc.identifier.endpage550
dc.identifier.issn0748-2337
dc.identifier.issn1477-0393
dc.identifier.issue3en_US
dc.identifier.pmid24193051
dc.identifier.scopus2-s2.0-84961258230
dc.identifier.scopusqualityQ3
dc.identifier.startpage541
dc.identifier.urihttps://doi.org/10.1177/0748233713504810
dc.identifier.urihttps://hdl.handle.net/20.500.11776/5747
dc.identifier.volume32
dc.identifier.wosWOS:000371603500016
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorÜnsal, Cüneyt
dc.institutionauthorAktaş, Cevat
dc.institutionauthorErboğa, Mustafa
dc.language.isoen
dc.publisherSage Publications Inc
dc.relation.ispartofToxicology and Industrial Health
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectCadmium
dc.subjectQuercetin
dc.subjecthippocampus
dc.subjectoxidative stress
dc.subjectneuronal damage
dc.subjectLipid-Peroxidation
dc.subjectCortical-Neurons
dc.subjectIn-Vitro
dc.subjectAntioxidant
dc.subjectStress
dc.subjectExposure
dc.subjectDeath
dc.subjectRats
dc.subjectPermeability
dc.subjectGlutathione
dc.titleNeuroprotective effect of quercetin against oxidative damage and neuronal apoptosis caused by cadmium in hippocampus
dc.typeArticle

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