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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleMangiferin, A Natural Occurring Glucosyl Xanthone, Increases Susceptibility Of Rat Liver Mitochondria To Calcium-induced Permeability Transition.pt_BR
dc.contributor.authorAndreu, Gilberto Lázaro Pardopt_BR
dc.contributor.authorDelgado, Renépt_BR
dc.contributor.authorVelho, Jesus Antoniopt_BR
dc.contributor.authorCurti, Carlospt_BR
dc.contributor.authorVercesi, Anibal Ept_BR
unicamp.authorGilberto Lázaro Pardo Andreu, Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas 13083-970 Campinas, SP, Brazil. g031071@yahoo.compt_BR
unicamp.author.externalRené Delgado,pt
unicamp.author.externalJesus Antonio Velho,pt
unicamp.author.externalCarlos Curti,pt
unicamp.author.externalAnibal E Vercesi,pt
dc.subjectAdenosine Diphosphatept_BR
dc.subjectAnimalspt_BR
dc.subjectCalciumpt_BR
dc.subjectCyclosporinept_BR
dc.subjectEgtazic Acidpt_BR
dc.subjectEthylmaleimidept_BR
dc.subjectGlutathionept_BR
dc.subjectHorseradish Peroxidasept_BR
dc.subjectIntracellular Membranespt_BR
dc.subjectLipid Peroxidationpt_BR
dc.subjectMalept_BR
dc.subjectMembrane Potentialspt_BR
dc.subjectMitochondria, Liverpt_BR
dc.subjectMitochondrial Swellingpt_BR
dc.subjectNadppt_BR
dc.subjectPermeabilitypt_BR
dc.subjectRatspt_BR
dc.subjectRats, Wistarpt_BR
dc.subjectReactive Oxygen Speciespt_BR
dc.subjectSulfhydryl Compoundspt_BR
dc.subjectXanthonespt_BR
dc.description.abstractMitochondrial permeability transition (MPT) is a Ca(2+)-dependent, cyclosporine A-sensitive, non-selective inner membrane permeabilization induced by a wide range of agents or conditions, which has often been associated with necrotic or apoptotic cell death. When mitochondria isolated from livers of rats treated with the natural occurring glucosyl xanthone mangiferin (40 mg/kg body weight) were exposed in vitro to Ca(2+), they underwent CsA, NEM, and ADP-sensitive high amplitude swelling and associated membrane potential dissipation, release of pre-accumulated Ca(2+), oxidation of thiol groups, and depletion of GSH, without changes in the NAD(P)H redox state. The same treatment reduced the phosphorylation rate of mitochondria and the resting respiration by around 4 and 11%, respectively, as well as generation of reactive oxygen species (ROS) by organelle. The in vitro exposure of untreated mitochondria to mangiferin plus Ca(2+) also resulted in oxidation of thiol groups, in the same way that the compound inhibited the Ca(2+)-induced peroxidation of mitochondrial membrane lipids. The spectrum of mangiferin during its oxidation by the H(2)O(2)/HRP system showed a characteristic absorption peak at 380 nm, which decreased immediately after reaction was started; two isosbestic points at around 336 and 412 nm, with a blue shift in the position of the maxima absorption of mangiferin were observed, suggesting their conversion into one oxidation product. Glutathione abolished this decrease of absorbance, suggesting that the oxidation product of mangiferin forms adducts with GSH. We propose that Ca(2+) increases levels of mitochondria-generated ROS, which reacts with mangiferin producing quinoid derivatives, which in turn react with the most accessible mitochondrial thiol groups, thus triggering MPT. It seems probable that the free radical scavenging activity of mangiferin shifts its anti-oxidant protection to the thiol arylation. An interesting proposition is that accumulation of mangiferin quinoid products would take place in cells exposed to an overproduction of ROS, such as cancer cells, where the occurrence of MPT-mediated apoptosis may be a cellular defence mechanism against excessive ROS formation.en
dc.relation.ispartofArchives Of Biochemistry And Biophysicspt_BR
dc.relation.ispartofabbreviationArch. Biochem. Biophys.pt_BR
dc.date.issued2005-Julpt_BR
dc.identifier.citationArchives Of Biochemistry And Biophysics. v. 439, n. 2, p. 184-93, 2005-Jul.pt_BR
dc.language.isoengpt_BR
dc.description.volume439pt_BR
dc.description.firstpage184-93pt_BR
dc.rightsfechadopt_BR
dc.rights.holderpt_BR
dc.sourcePubMedpt_BR
dc.identifier.issn0003-9861pt_BR
dc.identifier.doi10.1016/j.abb.2005.05.015pt_BR
dc.identifier.urlhttp://www.ncbi.nlm.nih.gov/pubmed/15979560pt_BR
dc.date.available2015-11-27T13:02:14Z-
dc.date.accessioned2015-11-27T13:02:14Z-
dc.description.provenanceMade available in DSpace on 2015-11-27T13:02:14Z (GMT). No. of bitstreams: 1 pmed_15979560.pdf: 978434 bytes, checksum: 30e7163ac39ceb8d8ebfc7c12a4cd0b2 (MD5) Previous issue date: 2005en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/196321-
dc.identifier.idPubmed15979560pt_BR
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