Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/5379
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dc.contributor.authorOliveira, Paulo J.-
dc.contributor.authorBjork, James A.-
dc.contributor.authorSantos, Maria S.-
dc.contributor.authorLeino, Richard L.-
dc.contributor.authorFroberg, M. Kent-
dc.contributor.authorMoreno, António J.-
dc.contributor.authorWallace, Kendall B.-
dc.date.accessioned2008-09-01T15:41:16Z-
dc.date.available2008-09-01T15:41:16Z-
dc.date.issued2004en_US
dc.identifier.citationToxicology and Applied Pharmacology. 200:2 (2004) 159-168en_US
dc.identifier.urihttp://hdl.handle.net/10316/5379-
dc.description.abstractThe cardiotoxicity associated with doxorubicin (DOX) therapy limits the total cumulative dose and therapeutic success of active anticancer chemotherapy. Cardiac mitochondria are implicated as primary targets for DOX toxicity, which is believed to be mediated by the generation of highly reactive free radical species of oxygen from complex I of the mitochondrial electron transport chain. The objective of this study was to determine if the protection demonstrated by carvedilol (CV), a [beta]-adrenergic receptor antagonist with strong antioxidant properties, against DOX-induced mitochondrial-mediated cardiomyopathy [Toxicol. Appl. Pharmacol. 185 (2002) 218] is attributable to its antioxidant properties or its [beta]-adrenergic receptor antagonism. Our results confirm that DOX induces oxidative stress, mitochondrial dysfunction, and histopathological lesions in the cardiac tissue, all of which are inhibited by carvedilol. In contrast, atenolol (AT), a [beta]-adrenergic receptor antagonist lacking antioxidant properties, preserved phosphate energy charge but failed to protect against any of the indexes of DOX-induced oxidative mitochondrial toxicity. We therefore conclude that the cardioprotective effects of carvedilol against DOX-induced mitochondrial cardiotoxicity are due to its inherent antioxidant activity and not to its [beta]-adrenergic receptor antagonism.en_US
dc.description.urihttp://www.sciencedirect.com/science/article/B6WXH-4CP69N9-2/1/af6fb8993cd9345f9ad3e7303bff3b0aen_US
dc.format.mimetypeaplication/PDFen
dc.language.isoengeng
dc.rightsopenAccesseng
dc.subjectMitochondriaen_US
dc.subjectDoxorubicinen_US
dc.subjectCarvedilolen_US
dc.subjectAtenololen_US
dc.subjectPermeability transition poreen_US
dc.subjectOxidative damageen_US
dc.subjectMitochondrionopathyen_US
dc.titleCarvedilol-mediated antioxidant protection against doxorubicin-induced cardiac mitochondrial toxicityen_US
dc.typearticleen_US
dc.identifier.doi10.1016/j.taap.2004.04.005-
uc.controloAutoridadeSim-
item.fulltextCom Texto completo-
item.grantfulltextopen-
item.languageiso639-1en-
crisitem.author.deptInstitute of Interdisciplinary Research-
crisitem.author.deptFaculty of Sciences and Technology-
crisitem.author.parentdeptUniversity of Coimbra-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitMARE - Marine and Environmental Sciences Centre-
crisitem.author.orcid0000-0002-5201-9948-
crisitem.author.orcid0000-0002-6881-9392-
crisitem.author.orcid0000-0003-3575-7604-
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais
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