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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleProtection of insulin-producing cells against toxicity of dexamethasone by catalase overexpressionpt_BR
dc.contributor.authorRoma, LPpt_BR
dc.contributor.authorBosqueiro, JRpt_BR
dc.contributor.authorCunha, DApt_BR
dc.contributor.authorCarneiro, EMpt_BR
dc.contributor.authorGurgul-Convey, Ept_BR
dc.contributor.authorLenzen, Spt_BR
dc.contributor.authorBoschero, ACpt_BR
dc.contributor.authorSouza, KLApt_BR
unicamp.authorRoma, Leticia P. Cunha, Daniel A. Carneiro, Everardo M. Boschero, Antonio C. Souza, Kleber L. A. Univ Estadual Campinas, Inst Biol, Dept Physiol & Biophys, BR-13083970 Campinas, SP, Brazilpt_BR
unicamp.authorBosqueiro, Jose R. Sao Paulo State Univ, Dept Phys Educ, Bauru, SP, Brazilpt_BR
unicamp.authorGurgul-Convey, Ewa Lenzen, Sigurd Hannover Med Sch, Inst Clin Biochem, D-3000 Hannover, Germanypt_BR
dc.subjectOxidative stresspt_BR
dc.subjectInsulin-secreting cellspt_BR
dc.subjectIslets of Langerhanspt_BR
dc.subjectDrug effectspt_BR
dc.subjectIn vitropt_BR
dc.subjectFree radicalspt_BR
dc.subjectHyPer Vectorpt_BR
dc.subject.wosEnzyme Gene-expressionpt_BR
dc.subject.wosOxidative Stresspt_BR
dc.subject.wosAntioxidant Enzymespt_BR
dc.subject.wosInduced Apoptosispt_BR
dc.subject.wosSecreting Cellspt_BR
dc.subject.wosRinm5f Cellspt_BR
dc.description.abstractPancreatic cells are very sensitive to reactive oxygen species (ROS) and this might play an important role in beta cell death in diabetes. Dexamethasone is a synthetic diabetogenic glucocorticoid, which impairs pancreatic beta cell function. Therefore we investigated the toxicity of dexamethasone in RINm5F insulin-producing cells and its dependence on the expression level of the antioxidant enzyme catalase, which inactivates hydrogen peroxide. This was correlated with oxidative stress and cell death. An increased generation of ROS was observed in dexamethasone-treated cells together with an increase in caspase-3 activity and apoptosis rate. Interestingly, exposure to dexamethasone increased the cytosolic superoxide dismutase Cu/ZnSOD protein expression and activity, whereas the mitochondrial MnSOD isoform was not affected by the glucocorticoid. Catalase overexpression in insulin-producing cells prevented all the cytotoxic effects of dexamethasone. In conclusion, dexamethasone-induced cell death in insulin-producing cells is ROS mediated. Increased levels of expression and activity of the Cu/ZnSOD might favor the generation of hydrogen peroxide in dexamethasone-treated cells. Increased ROS scavenging capacity in insulin-producing cells, through overexpression of catalase, prevents a deleterious increase in hydrogen peroxide generation and thus prevents dexamethasone-induced apoptosis. (C) 2009 Elsevier Inc. All rights
dc.relation.ispartofFree Radical Biology And Medicinept_BR
dc.relation.ispartofabbreviationFree Radic. Biol. Med.pt_BR
dc.publisher.cityNew Yorkpt_BR
dc.publisherElsevier Science Incpt_BR
dc.identifier.citationFree Radical Biology And Medicine. Elsevier Science Inc, v. 47, n. 10, n. 1386, n. 1393, 2009.pt_BR
dc.sourceWeb of Sciencept_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipEuropean Union [LSHM-CT-2006-518153, LSHM-CT-2006-036903]pt_BR
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorship1Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.description.sponsordocumentnumberEuropean Union [LSHM-CT-2006-518153, LSHM-CT-2006-036903]pt
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