Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348430
Full metadata record
DC FieldValueLanguage
dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampVercesi, Anibal Eugenio-
dc.contributor.authorunicampInada, Natalia Mayumi-
dc.typeArtigopt_BR
dc.titleUncoupling and oxidative stress in liver mitochondria isolated from rats with acute iron overloadpt_BR
dc.contributor.authorAndreu, G. L. Pardo-
dc.contributor.authorInada, N. M.-
dc.contributor.authorVercesi, A. E.-
dc.contributor.authorCurti, C.-
dc.subjectSobrecarga de ferropt_BR
dc.subjectMitocôndriapt_BR
dc.subject.otherlanguageIron overloadpt_BR
dc.subject.otherlanguageMitochondriapt_BR
dc.description.abstractOne hypothesis for the etiology of cell damage arising from iron overload is that its excess selectively affects mitochondria. Here we tested the effects of acute iron overload on liver mitochondria isolated from rats subjected to a single dose of i.p. 500 mg/kg iron–dextran. The treatment increased the levels of iron in mitochondria (from 21 ± 4 to 130 ± 7 nmol/mg protein) and caused both lipid peroxidation and glutathione oxidation. The mitochondria of iron-treated rats showed lower respiratory control ratio in association with higher resting respiration. The mitochondrial uncoupling elicited by iron-treatment did not affect the phosphorylation efficiency or the ATP levels, suggesting that uncoupling is a mitochondrial protective mechanism against acute iron overload. Therefore, the reactive oxygen species (ROS)/H+ leak couple, functioning as a mitochondrial redox homeostatic mechanism could play a protective role in the acutely iron-loaded mitochondriapt_BR
dc.relation.ispartofArchives of toxicologypt_BR
dc.relation.ispartofabbreviationArch. toxicol.pt_BR
dc.publisher.cityHeidelbergpt_BR
dc.publisher.countryAlemanhapt_BR
dc.publisherSpringerpt_BR
dc.date.issued2009-
dc.language.isoengpt_BR
dc.description.volume83pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0340-5761pt_BR
dc.identifier.eissn1432-0738pt_BR
dc.identifier.doi10.1007/s00204-008-0322-xpt_BR
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs00204-008-0322-xpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumbernão tempt_BR
dc.date.available2020-09-01T13:29:11Z-
dc.date.accessioned2020-09-01T13:29:11Z-
dc.description.provenanceSubmitted by Mariana Aparecida Azevedo (mary1@unicamp.br) on 2020-09-01T13:29:11Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:14:48Z : No. of bitstreams: 1 000262410600007.pdf: 461094 bytes, checksum: b34f0cb961f8601efa4b12ee156f6fbf (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-01T13:29:11Z (GMT). No. of bitstreams: 0 Previous issue date: 2009en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348430-
dc.contributor.departmentDepartamento de Patologia Clínicapt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordOxidative stresspt_BR
dc.subject.keywordReactive oxygen species (ROS)pt_BR
dc.subject.keywordUncouplingpt_BR
dc.identifier.source000262410600007pt_BR
dc.creator.orcid0000-0002-0504-5676pt_BR
dc.creator.orcid0000-0003-1940-186Xpt_BR
dc.type.formArtigopt_BR
dc.identifier.articleid47pt_BR
Appears in Collections:FCM - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
000262410600007.pdf450.29 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.