Effects Of Partial Inhibition Of Respiratory Complex I On H2o2 Production By Isolated Brain Mitochondria In Different Respiratory States

dc.creatorMichelini L.G.B.
dc.creatorBenevento C.E.
dc.creatorRossato F.A.
dc.creatorSiqueira-Santos E.S.
dc.creatorCastilho R.F.
dc.date2014
dc.date2015-06-25T18:03:53Z
dc.date2015-11-26T15:06:11Z
dc.date2015-06-25T18:03:53Z
dc.date2015-11-26T15:06:11Z
dc.date.accessioned2018-03-28T22:16:42Z
dc.date.available2018-03-28T22:16:42Z
dc.identifier
dc.identifierNeurochemical Research. Springer New York Llc, v. 39, n. 12, p. 2419 - 2430, 2014.
dc.identifier3643190
dc.identifier10.1007/s11064-014-1446-4
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84912527524&partnerID=40&md5=bf7f87f01196fed164fdd54b6b286ce5
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/88083
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/88083
dc.identifier2-s2.0-84912527524
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1257194
dc.descriptionThe 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 ± 1.0 to 26.4 ± 2.6 nmol O2 mg−1 min−1 and from 7.8 ± 0.3 to 6.3 ± 0.3 nmol O2 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 ± 1.1 to 21.0 ± 1.2 pmol H2O2 mg−1 min−1 and 56.5 ± 4.7 to 95.0 ± 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 conditions.
dc.description39
dc.description12
dc.description2419
dc.description2430
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dc.languageen
dc.publisherSpringer New York LLC
dc.relationNeurochemical Research
dc.rightsfechado
dc.sourceScopus
dc.titleEffects Of Partial Inhibition Of Respiratory Complex I On H2o2 Production By Isolated Brain Mitochondria In Different Respiratory States
dc.typeArtículos de revistas


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