Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection

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dc.contributor.authorDincel, Gungor Cagdas
dc.contributor.authorAtmaca, Hasan Tarik
dc.date.accessioned2020-06-25T18:16:32Z
dc.date.available2020-06-25T18:16:32Z
dc.date.issued2016
dc.departmentKırıkkale Üniversitesi
dc.descriptionDINCEL, Gungor Cagdas/0000-0002-6985-3197; ATMACA, HASAN TARIK/0000-0001-8379-4114
dc.description.abstractOxidative stress (OS) plays an essential role in the pathogenesis of common neurodegenerative diseases. We have previously shown that Toxoplasma gondii (T. gondii) induces high nitric oxide (NO) production, glial activation, and apoptosis that altogether cause severe neuropathology in toxoplasma encephalitis (TE). The objective of this study was to investigate the cytotoxic effect of OS and to identify a correlation between the causes of T. gondii induced neuropathology. Expression levels of glutathione reductase (GR), Cu/Zn superoxide dismutase (SOD1), neuron specific enolase (NSE), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were investigated. Results of the study revealed that the levels of GR (P <0.005) and NSE (P<0.001) expression in the brain tissue markedly increased while SOD1 activity decreased (P<0.001) in the infected group compared to the non-infected group. In addition, intense staining for 8-OHdG (P<0.05) was observed both in the nucleus and the cytoplasm of neurons and glial cells that underwent OS. These results were reasonable to suggest that T. gondii-mediated OS might play a pivotal role and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of TE. The results also clearly indicated that increased levels of NO and apoptosis might contribute to OS-related pathogenesis of TE. As a result, OS and expression of NSE might give an idea of the disease progress and may have a critical diagnostic significance for patients with T. gondii infection.en_US
dc.description.sponsorshipScientific Research Projects Commission of the Gumushane Univesity, Gumushane, Turkey [13.B0421.02.02]en_US
dc.description.sponsorshipThis work was funded and supported by the Scientific Research Projects Commission of the Gumushane Univesity, Gumushane, Turkey (Project Code: 13.B0421.02.02).en_US
dc.identifier.citationDincel GC, Atmaca HT. Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection. International Journal of Immunopathology and Pharmacology. 2016;29(2):226-240.en_US
dc.identifier.doi10.1177/0394632016638668
dc.identifier.endpage240en_US
dc.identifier.issn2058-7384
dc.identifier.issue2en_US
dc.identifier.pmid26966143
dc.identifier.scopus2-s2.0-84966702161
dc.identifier.scopusqualityQ3
dc.identifier.startpage226en_US
dc.identifier.urihttps://doi.org/10.1177/0394632016638668
dc.identifier.urihttps://hdl.handle.net/20.500.12587/6558
dc.identifier.volume29en_US
dc.identifier.wosWOS:000375028200009
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSage Publications Incen_US
dc.relation.ispartofInternational Journal Of Immunopathology And Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subject8-OHdGen_US
dc.subjectneuron specific enolaseen_US
dc.subjectneuropathologyen_US
dc.subjectoxidative stressen_US
dc.subjectToxoplasma gondiien_US
dc.titleRole of oxidative stress in the pathophysiology of Toxoplasma gondii infectionen_US
dc.typeArticle

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