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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampMichelini, Luiz Guilherme Bueno-
dc.contributor.authorunicampRossato, Franco Aparecido-
dc.contributor.authorunicampCastilho, Roger Frigério-
dc.typeArtigopt_BR
dc.titleEffects of partial inhibition of respiratory complex I on H2o2 production by isolated brain mitochondria in different respiratory statespt_BR
dc.contributor.authorMichelini, Luiz G. B.-
dc.contributor.authorBenevento, Carlos E.-
dc.contributor.authorRossato, Franco A.-
dc.contributor.authorSiqueira-Santos, Edilene S.-
dc.contributor.authorCastilho, Roger F.-
dc.subjectDoença de Parkinsonpt_BR
dc.subjectRotenonapt_BR
dc.subject.otherlanguageParkinson diseasept_BR
dc.subject.otherlanguageRotenonept_BR
dc.description.abstractThe aim of this work was to characterize the effects of partial inhibition of respiratory complex I by rotenone on H2O2 production by isolated rat brain mitochondria in different respiratory states. Flow cytometric analysis of membrane potential in isolated mitochondria indicated that rotenone leads to uniform respiratory inhibition when added to a suspension of mitochondria. When mitochondria were incubated in the presence of a low concentration of rotenone (10 nm) and NADH-linked substrates, oxygen consumption was reduced from 45.9 +/- A 1.0 to 26.4 +/- A 2.6 nmol O-2 mg(-1) min(-1) and from 7.8 +/- A 0.3 to 6.3 +/- A 0.3 nmol O-2 mg(-1) min(-1) in respiratory states 3 (ADP-stimulated respiration) and 4 (resting respiration), respectively. Under these conditions, mitochondrial H2O2 production was stimulated from 12.2 +/- A 1.1 to 21.0 +/- A 1.2 pmol H2O2 mg(-1) min(-1) and 56.5 +/- A 4.7 to 95.0 +/- A 11.1 pmol H2O2 mg(-1) min(-1) in respiratory states 3 and 4, respectively. Similar results were observed when comparing mitochondrial preparations enriched with synaptic or nonsynaptic mitochondria or when 1-methyl-4-phenylpyridinium ion (MPP+) was used as a respiratory complex I inhibitor. Rotenone-stimulated H2O2 production in respiratory states 3 and 4 was associated with a high reduction state of endogenous nicotinamide nucleotides. In succinate-supported mitochondrial respiration, where most of the mitochondrial H2O2 production relies on electron backflow from complex II to complex I, low rotenone concentrations inhibited H2O2 production. Rotenone had no effect on mitochondrial elimination of micromolar concentrations of H2O2. The present results support the conclusion that partial complex I inhibition may result in mitochondrial energy crisis and oxidative stress, the former being predominant under oxidative phosphorylation and the latter under resting respiration conditionspt_BR
dc.relation.ispartofNeurochemical Researchpt_BR
dc.relation.ispartofabbreviationNeurochem. Res.pt_BR
dc.publisher.cityNew York, NYpt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherSpringerpt_BR
dc.date.issued2014-
dc.date.monthofcirculationDec.pt_BR
dc.language.isoengpt_BR
dc.description.volume39pt_BR
dc.description.issuenumber12pt_BR
dc.description.firstpage2419pt_BR
dc.description.lastpage2430pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0364-3190pt_BR
dc.identifier.eissn1573-6903pt_BR
dc.identifier.doi10.1007/s11064-014-1446-4pt_BR
dc.identifier.doi10.1007/s11064-015-1518-0pt_BR
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs11064-014-1446-4pt_BR
dc.identifier.urlhttps://link.springer.com/article/10.1007/s11064-015-1518-0pt_BR
dc.description.sponsorshipCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQpt_BR
dc.description.sponsorshipCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.description.sponsordocumentnumber2011/50400-0; 2011/14229-4pt_BR
dc.date.available2021-01-11T15:42:57Z-
dc.date.accessioned2021-01-11T15:42:57Z-
dc.description.provenanceSubmitted by Cintia Oliveira de Moura (cintiaom@unicamp.br) on 2021-01-11T15:42:57Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-02-19T19:00:02Z : No. of bitstreams: 1 000345645700015.pdf: 671733 bytes, checksum: 7508aa882ec2944778fc67d75d124fe1 (MD5). Added 1 bitstream(s) on 2021-02-19T19:00:03Z : No. of bitstreams: 2 000345645700015.pdf: 671733 bytes, checksum: 7508aa882ec2944778fc67d75d124fe1 (MD5) 000351861100025.pdf: 166908 bytes, checksum: 6b88af57f8e468b3fb16d79a1977eb3a (MD5)en
dc.description.provenanceMade available in DSpace on 2021-01-11T15:42:57Z (GMT). No. of bitstreams: 0 Previous issue date: 2014en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/353841-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Patologia Clínicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000345645700015pt_BR
dc.identifier.source000351861100025pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0002-4132-2271pt_BR
dc.creator.orcid0000-0003-2338-8717pt_BR
dc.type.formArtigo originalpt_BR
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