Beneficial effects of nontoxic ozone on H2O2-induced stress and inflammation

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dc.contributor.authorKucukgul, Altug
dc.contributor.authorErdogan, Suat
dc.contributor.authorGonenci, Ramazan
dc.contributor.authorOzan, Gonca
dc.date.accessioned2024-06-12T11:11:54Z
dc.date.available2024-06-12T11:11:54Z
dc.date.issued2016
dc.departmentTrakya Üniversitesien_US
dc.description58th Annual Meeting of the Canadian-Society-for-Molecular-Biosciences (CSMB) -- JUN 14-17, 2015 -- Halifax, CANADAen_US
dc.description.abstractIn this study, the anti-oxidant and anti-inflammatory efficacy of ozone oxidative preconditioning (OOP) were investigated on hydrogen peroxide (H2O2)-induced human lung alveolar cells. In MTT and trypan blue viability tests, while 100 mu mol/L H2O2 caused a 17.3% and 21.9% decrease in the number of living cells, respectively, ozone at 20 mu mol/L regenerated cell proliferation and prevented 9.6% and 11.0% of cell loss, respectively. In addition, H2O2 decreased the transcription levels of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) 5.43-, 2.89-, and 5.33-fold, respectively, while it increased Bax, NF-kappa beta, TNF-alpha, and iNOS expression 1.57-, 1.32-, 1.40-, and 1.41-fold, respectively. Ozone pretreatment, however, increased CAT, GPx, and SOD transcription levels 7.08-, 5.17-, and 6.49-fold and decreased Bax, NF-kappa beta, TNF-alpha, and iNOS transcriptions by 1.25-, 0.76-, 3.63-, and 7.91-fold, respectively. Moreover, intracellular glutathione (GSH) level and SOD activity were decreased by 46.2% and 45.0% in the H2O2 treatment group, and OOP recovered 58.5% and 20.1% of the decreases caused by H2O2. H2O2 also increased nitrite levels 7.84-fold, and OOP reduced this increase by half. Consequently, OOP demonstrated potent anti-oxidant and anti-inflammatory effects on in vitro model of oxidative stress-induced lung injury.en_US
dc.description.sponsorshipCanadian Soc Mol Biosciencesen_US
dc.identifier.doi10.1139/bcb-2016-0033
dc.identifier.endpage583en_US
dc.identifier.issn0829-8211
dc.identifier.issn1208-6002
dc.identifier.issue6en_US
dc.identifier.pmid27842206en_US
dc.identifier.scopus2-s2.0-84995931575en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage577en_US
dc.identifier.urihttps://doi.org/10.1139/bcb-2016-0033
dc.identifier.urihttps://hdl.handle.net/20.500.14551/22972
dc.identifier.volume94en_US
dc.identifier.wosWOS:000388092900010en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherCanadian Science Publishingen_US
dc.relation.ispartofBiochemistry And Cell Biologyen_US
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectOxidative Stressen_US
dc.subjectInflammationen_US
dc.subjectOzone Oxidative Preconditioningen_US
dc.subjectLung Alveolar Cellsen_US
dc.subjectOxidative Stressen_US
dc.subjectReactive Oxygenen_US
dc.subjectCanceren_US
dc.subjectDamageen_US
dc.subjectCellsen_US
dc.subjectIschemia/Reperfusionen_US
dc.subjectApoptosisen_US
dc.subjectInjuryen_US
dc.titleBeneficial effects of nontoxic ozone on H2O2-induced stress and inflammationen_US
dc.typeConference Objecten_US

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