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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleOxidative Stress In Ca(2+)-induced Membrane Permeability Transition In Brain Mitochondria.pt_BR
dc.contributor.authorMaciel, E Npt_BR
dc.contributor.authorVercesi, A Ept_BR
dc.contributor.authorCastilho, R Fpt_BR
unicamp.authorE N Maciel, Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, Brazil.pt_BR
unicamp.author.externalA E Vercesi,pt
unicamp.author.externalR F Castilho,pt
dc.subjectAnimalspt_BR
dc.subjectAntioxidantspt_BR
dc.subjectBrainpt_BR
dc.subjectCalciumpt_BR
dc.subjectCalcium Signalingpt_BR
dc.subjectCatalasept_BR
dc.subjectCell Membrane Permeabilitypt_BR
dc.subjectChelating Agentspt_BR
dc.subjectEgtazic Acidpt_BR
dc.subjectFluoresceinspt_BR
dc.subjectFluorescent Dyespt_BR
dc.subjectFree Radicalspt_BR
dc.subjectLipid Peroxidationpt_BR
dc.subjectMembrane Potentialspt_BR
dc.subjectMitochondriapt_BR
dc.subjectNadppt_BR
dc.subjectNeuronspt_BR
dc.subjectOxidative Stresspt_BR
dc.subjectRatspt_BR
dc.subjectRats, Wistarpt_BR
dc.subjectReactive Oxygen Speciespt_BR
dc.subjectSodiumpt_BR
dc.description.abstractMitochondrial permeability transition (PT) is a non-selective inner membrane permeabilization, typically promoted by the accumulation of excessive quantities of Ca(2+) ions in the mitochondrial matrix. This phenomenon may contribute to neuronal cell death under some circumstances, such as following brain trauma and hypoglycemia. In this report, we show that Ca(2+)-induced brain mitochondrial PT was stimulated by Na(+) (10 mM) and totally prevented by the combination of ADP and cyclosporin A. Removal of Ca(2+) from the mitochondrial suspension by EGTA or inhibition of Ca(2+) uptake by ruthenium red partially reverted the dissipation of the membrane potential associated with PT. Ca(2+)-induced brain mitochondrial PT was significantly inhibited by the antioxidant catalase, indicating the participation of reactive oxygen species in this process. An increased detection of reactive oxygen species, measured through dichlorodihydrofluorescein oxidation, was observed after mitochondrial Ca(2+) uptake. Ca(2+)-induced dichlorodihydrofluorescein oxidation was enhanced by Na(+) and prevented by ADP and cyclosporin A, indicating that PT enhances mitochondrial oxidative stress. This could be at least in part a consequence of the extensive depletion in NAD(P)H that accompanied this Ca(2+)-induced mitochondrial PT. NADPH is known to maintain the antioxidant function of the glutathione reductase/peroxidase and thioredoxin reductase/peroxidase systems. In addition, the occurrence of mitochondrial PT was associated with membrane lipid peroxidation. We conclude that PT further increases Ca(2+)-induced oxidative stress in brain mitochondria leading to secondary damage such as lipid peroxidation.en
dc.relation.ispartofJournal Of Neurochemistrypt_BR
dc.relation.ispartofabbreviationJ. Neurochem.pt_BR
dc.date.issued2001-Decpt_BR
dc.identifier.citationJournal Of Neurochemistry. v. 79, n. 6, p. 1237-45, 2001-Dec.pt_BR
dc.language.isoengpt_BR
dc.description.volume79pt_BR
dc.description.firstpage1237-45pt_BR
dc.rightsfechadopt_BR
dc.rights.holderpt_BR
dc.sourcePubMedpt_BR
dc.identifier.issn0022-3042pt_BR
dc.identifier.doipt_BR
dc.identifier.urlhttp://www.ncbi.nlm.nih.gov/pubmed/11752064pt_BR
dc.date.available2015-11-27T12:29:06Z-
dc.date.accessioned2015-11-27T12:29:06Z-
dc.description.provenanceMade available in DSpace on 2015-11-27T12:29:06Z (GMT). No. of bitstreams: 1 pmed_11752064.pdf: 311363 bytes, checksum: ecab8958a8a1f121c9242b3726695498 (MD5) Previous issue date: 2001en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/194907-
dc.identifier.idPubmed11752064pt_BR
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