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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleYeast oxidative stress response - Influences of cytosolic thioredoxin peroxidase I and of the mitochondrial functional statept_BR
dc.contributor.authorDemasi, APDpt_BR
dc.contributor.authorPereira, GAGpt_BR
dc.contributor.authorNetto, LESpt_BR
unicamp.authorUniv Estadual Campinas, Dept Genet & Evolucao IB, Lab Genom & Expressao IB, BR-13083970 Campinas, SP, Brazil Univ Sao Paulo, Dept Genet & Biol Evolut, IB, Sao Paulo, Brazilpt_BR
dc.subjecthydrogen peroxidept_BR
dc.subjectgene expressionpt_BR
dc.subjectmitochondrial dysfunctionpt_BR
dc.subjectoxidative stresspt_BR
dc.subjectthioredoxin peroxidasept_BR
dc.subject.wosYap1 Transcription Factorpt_BR
dc.subject.wos2-cys Peroxiredoxinpt_BR
dc.subject.wosAntioxidant Defensept_BR
dc.subject.wosThiol Peroxidasept_BR
dc.subject.wosBudding Yeastpt_BR
dc.description.abstractWe investigated the changes in the oxidative stress response of yeast cells suffering mitochondrial dysfunction that could impair their viability. First, we demonstrated that cells with this dysfunction rely exclusively on cytosolic thioredoxin peroxidase I (cTPxI) and its reductant sulfiredoxin, among other antioxidant enzymes tested, to protect them against H2O2-induced death. This cTPxI-dependent protection could be related to its dual functions, as peroxidase and as molecular chaperone, suggested by mixtures of low and high molecular weight oligomeric structures of cTPxI observed in cells challenged with H2O2. We found that cTPxI deficiency leads to increased basal sulfhydryl levels and transcriptional activation of most of the H2O2-responsive genes, interpreted as an attempt by the cells to improve their antioxidant defense. On the other hand, mitochondrial dysfunction, specifically the electron transport blockage, provoked a huge depletion of sulfhydryl groups after H2O2 treatment and reduced the H2O2-mediated activation of some genes otherwise observed, impairing cell defense and viability. The transcription factors Yap1 and Skn7 are crucial for the antioxidant response of cells under inhibited electron flow condition and probably act in the same pathway of cTPxI to protect cells affected by this disorder. Yap1 cellular distribution was not affected by cTpxI deficiency and by mitochondrial dysfunction, in spite of the observed expression alterations of several Yap1-target genes, indicating alternative mechanisms of Yap1 activation/deactivation. Therefore, we propose that cTPxI is specifically important in the protection of yeast with mitochondrial dysfunction due to its functional versatility as an antioxidant, chaperone and modulator of gene
dc.relation.ispartofFebs Journalpt_BR
dc.relation.ispartofabbreviationFEBS J.pt_BR
dc.publisherBlackwell Publishingpt_BR
dc.identifier.citationFebs Journal. Blackwell Publishing, v. 273, n. 4, n. 805, n. 816, 2006.pt_BR
dc.sourceWeb of Sciencept_BR
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