Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/199643
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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleThe Higher Susceptibility Of Congenital Analbuminemic Rats To Ca2+-induced Mitochondrial Permeability Transition Is Associated With The Increased Expression Of Cyclophilin D And Nitrosothiol Depletion.pt_BR
dc.contributor.authorFigueira, Tiago Rpt_BR
dc.contributor.authorCastilho, Roger Fpt_BR
dc.contributor.authorSaito, Angelapt_BR
dc.contributor.authorOliveira, Helena C Fpt_BR
dc.contributor.authorVercesi, Anibal Ept_BR
unicamp.authorTiago R Figueira, Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.pt_BR
unicamp.author.externalRoger F Castilho,pt
unicamp.author.externalAngela Saito,pt
unicamp.author.externalHelena C F Oliveira,pt
unicamp.author.externalAnibal E Vercesi,pt
dc.subjectAnimalspt_BR
dc.subjectBrainpt_BR
dc.subjectCalciumpt_BR
dc.subjectCongenital Abnormalitiespt_BR
dc.subjectCyclophilinspt_BR
dc.subjectFemalept_BR
dc.subjectGene Expressionpt_BR
dc.subjectLiverpt_BR
dc.subjectMalept_BR
dc.subjectMembrane Potential, Mitochondrialpt_BR
dc.subjectMitochondriapt_BR
dc.subjectMitochondrial Swellingpt_BR
dc.subjectOxidative Stresspt_BR
dc.subjectPermeabilitypt_BR
dc.subjectRatspt_BR
dc.subjectRats, Sprague-dawleypt_BR
dc.subjectReactive Oxygen Speciespt_BR
dc.subjectS-nitrosothiolspt_BR
dc.subjectSerum Albuminpt_BR
dc.description.abstractCongenital analbuminemia is a rare autosomal recessive disorder characterized by a trace level of albumin in blood plasma and mild clinical symptoms. Analbuminemic patients generally present associated abnormalities, among which dyslipidemia is a hallmark. In this study, we show that mitochondria isolated from different tissues (liver, heart and brain) from 3-month-old analbuminemic rats (NAR) present a higher susceptibility to Ca(2+)-induced mitochondrial permeability transition (MPT), as assessed by either Ca(2+)-induced mitochondrial swelling, dissipation of membrane potential or mitochondrial Ca(2+) release. The Ca(2+) retention capacity of the liver mitochondria isolated from 3-month-old NAR was about 50% that of the control. Interestingly, the assessment of this variable in 21-day-old NAR indicated that the mitochondrial Ca(2+) retention capacity was preserved at this age, as compared to age-matched controls, which indicates that a reduced capacity for mitochondrial Ca(2+) retention is not a constitutive feature. The search for putative mediators of MPT sensitization in NAR revealed a 20% decrease in mitochondrial nitrosothiol content and a 30% increase in cyclophilin D expression. However, the evaluation of other variables related to mitochondrial redox status showed similar results between the controls and NAR, i.e., namely the contents of reduced mitochondrial membrane protein thiol groups and total glutathione, H(2)O(2) release rate, and NAD(P)H reduced state. We conclude that the higher expression of cyclophilin D, a major component of the MPT pore, and decreased nitrosothiol content in NAR mitochondria may underlie MPT sensitization in these animals.en
dc.relation.ispartofMolecular Genetics And Metabolismpt_BR
dc.relation.ispartofabbreviationMol. Genet. Metab.pt_BR
dc.date.issued2011-Decpt_BR
dc.identifier.citationMolecular Genetics And Metabolism. v. 104, n. 4, p. 521-8, 2011-Dec.pt_BR
dc.language.isoengpt_BR
dc.description.volume104pt_BR
dc.description.firstpage521-8pt_BR
dc.rightsfechadopt_BR
dc.rights.holderCopyright © 2011 Elsevier Inc. All rights reserved.pt_BR
dc.sourcePubMedpt_BR
dc.identifier.issn1096-7206pt_BR
dc.identifier.doi10.1016/j.ymgme.2011.08.031pt_BR
dc.identifier.urlhttp://www.ncbi.nlm.nih.gov/pubmed/21963200pt_BR
dc.date.available2015-11-27T13:21:55Z-
dc.date.accessioned2015-11-27T13:21:55Z-
dc.description.provenanceMade available in DSpace on 2015-11-27T13:21:55Z (GMT). No. of bitstreams: 1 pmed_21963200.pdf: 694005 bytes, checksum: 216cd09c327dc83eaa04e24950f60d2e (MD5) Previous issue date: 2011en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/199643-
dc.identifier.idPubmed21963200pt_BR
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