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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleInhibitory Effects Of Adenine Nucleotides On Brain Mitochondrial Permeability Transition.pt_BR
dc.contributor.authorSaito, Angelapt_BR
dc.contributor.authorCastilho, Roger Fpt_BR
unicamp.authorAngela Saito, Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.pt_BR
unicamp.author.externalRoger F Castilho,pt
dc.subjectAdenosine Diphosphatept_BR
dc.subjectAdenosine Triphosphatept_BR
dc.subjectAnimalspt_BR
dc.subjectBrainpt_BR
dc.subjectBrain Ischemiapt_BR
dc.subjectCalciumpt_BR
dc.subjectCytochromes Cpt_BR
dc.subjectFemalept_BR
dc.subjectMitochondriapt_BR
dc.subjectMitochondrial Swellingpt_BR
dc.subjectOxidative Phosphorylationpt_BR
dc.subjectRatspt_BR
dc.subjectRats, Wistarpt_BR
dc.description.abstractThe adenine nucleotides ADP and ATP are probably the most important endogenous inhibitors of the mitochondrial permeability transition (MPT). We studied the inhibitory effects of adenine nucleotides on brain MPT by measuring mitochondrial swelling and Ca(2+) and cytochrome c release. We observed that in the presence of either ADP or ATP, at 250 μM, brain mitochondria accumulated more than 1 μmol Ca(2+) × mg protein(-1). ADP or ATP also prevented Ca(2+)-induced mitochondrial swelling and cytochrome c release. Interestingly, ATP lost most of its inhibitory effects on MPT when the experiments were carried out in the presence of ATP-regenerating systems. These results indicate that MPT inhibition observed in the presence of added ATP could be mainly due to hydrolysis of ATP to ADP. From mitochondrial swelling measurements, half-maximal inhibitory values (K(i)) of 4.5 and 98 μM were obtained for ADP and ATP, respectively. In addition, a delayed mitochondrial swelling sensitive to higher ADP concentrations was observed. Mitochondrial anoxia/reoxygenation did not interfere with the inhibitory effect of ADP on Ca(2+)-induced MPT, but oxidative phosphorylation markedly decreased this effect. We conclude that ADP is a potent inhibitor of brain MPT whereas ATP is a weaker inhibitor of this phenomenon. Our results suggest that ADP can have an important protective role against MPT-mediated tissue damage under conditions of brain ischemia and hypoglycemia.en
dc.relation.ispartofNeurochemical Researchpt_BR
dc.relation.ispartofabbreviationNeurochem. Res.pt_BR
dc.date.issued2010-Novpt_BR
dc.identifier.citationNeurochemical Research. v. 35, n. 11, p. 1667-74, 2010-Nov.pt_BR
dc.language.isoengpt_BR
dc.description.volume35pt_BR
dc.description.firstpage1667-74pt_BR
dc.rightsfechadopt_BR
dc.sourcePubMedpt_BR
dc.identifier.issn1573-6903pt_BR
dc.identifier.doi10.1007/s11064-010-0228-xpt_BR
dc.identifier.urlhttp://www.ncbi.nlm.nih.gov/pubmed/20652632pt_BR
dc.date.available2015-11-27T13:18:05Z-
dc.date.accessioned2015-11-27T13:18:05Z-
dc.description.provenanceMade available in DSpace on 2015-11-27T13:18:05Z (GMT). No. of bitstreams: 1 pmed_20652632.pdf: 430463 bytes, checksum: d7772ff22bba718e95e19b2e337945d6 (MD5) Previous issue date: 2010en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/198965-
dc.identifier.idPubmed20652632pt_BR
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