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dc.contributor.authorRoma, Leticia P.-
dc.contributor.authorBosqueiro, José Roberto-
dc.contributor.authorCunha, Daniel A.-
dc.contributor.authorCarneiro, Everardo M.-
dc.contributor.authorGurgul-Convey, Ewa-
dc.contributor.authorLenzen, Sigurd-
dc.contributor.authorBoschero, Antonio C.-
dc.contributor.authorSouza, Kleber L. A.-
dc.date.accessioned2014-05-20T13:26:06Z-
dc.date.accessioned2016-10-25T16:46:19Z-
dc.date.available2014-05-20T13:26:06Z-
dc.date.available2016-10-25T16:46:19Z-
dc.date.issued2009-11-15-
dc.identifierhttp://dx.doi.org/10.1016/j.freeradbiomed.2009.08.010-
dc.identifier.citationFree Radical Biology and Medicine. New York: Elsevier B.V., v. 47, n. 10, p. 1386-1393, 2009.-
dc.identifier.issn0891-5849-
dc.identifier.urihttp://hdl.handle.net/11449/8361-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/8361-
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 B.V. All rights reserved.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
dc.description.sponsorshipEuropean Union-
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)-
dc.format.extent1386-1393-
dc.language.isoeng-
dc.publisherElsevier B.V.-
dc.sourceWeb of Science-
dc.subjectOxidative stressen
dc.subjectGlucocorticoidsen
dc.subjectCaspasesen
dc.subjectNecrosisen
dc.subjectInsulin-secreting cellsen
dc.subjectIslets of Langerhansen
dc.subjectDrug effectsen
dc.subjectPharmacologyen
dc.subjectIn vitroen
dc.subjectFree radicalsen
dc.subjectHyperProteinen
dc.subjectHyPer Vectoren
dc.titleProtection of insulin-producing cells against toxicity of dexamethasone by catalase overexpressionen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionHannover Med Sch-
dc.description.affiliationUniv Estadual Campinas, Inst Biol, Dept Physiol & Biophys, BR-13083970 Campinas, SP, Brazil-
dc.description.affiliationSão Paulo State Univ, Dept Phys Educ, Bauru, SP, Brazil-
dc.description.affiliationHannover Med Sch, Inst Clin Biochem, D-3000 Hannover, Germany-
dc.description.affiliationUnespSão Paulo State Univ, Dept Phys Educ, Bauru, SP, Brazil-
dc.description.sponsorshipIdEU: LSHM-CT-2006-518153-
dc.description.sponsorshipIdEU: LSHM-CT-2006-036903-
dc.identifier.doi10.1016/j.freeradbiomed.2009.08.010-
dc.identifier.wosWOS:000271934400008-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofFree Radical Biology and Medicine-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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