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dc.contributor.authorGranados Principal, Sergio
dc.contributor.authorEl-azem, Nuri
dc.contributor.authorPamplona Gras, Reinald
dc.contributor.authorRamirez Tortosa, Cesar
dc.contributor.authorPulido Moran, Mario
dc.contributor.authorVera Ramirez, Laura
dc.contributor.authorQuiles, Jose L.
dc.contributor.authorSánchez Rovira, Pedro
dc.contributor.authorNaudí i Farré, Alba
dc.contributor.authorPortero Otín, Manuel
dc.contributor.authorPérez López, Patricia
dc.contributor.authorRamírez Tortosa, MCarmen
dc.date.accessioned2016-11-10T10:50:58Z
dc.date.issued2014
dc.identifier.issn0006-2952
dc.identifier.urihttp://hdl.handle.net/10459.1/58464
dc.description.abstractOxidative stress is involved in several processes including cancer, aging and cardiovascular disease, and has been shown to potentiate the therapeutic effect of drugs such as doxorubicin. Doxorubicin causes significant cardiotoxicity characterized by marked increases in oxidative stress and mitochondrial dysfunction. Herein, we investigate whether doxorubicin-associated chronic cardiac toxicity can be ameliorated with the antioxidant hydroxytyrosol in rats with breast cancer. Thirty-six rats bearing breast tumors induced chemically were divided into 4 groups: control, hydroxytyrosol (0.5 mg/kg, 5 days/week), doxorubicin (1 mg/kg/week), and doxorubicin plus hydroxytyrosol. Cardiac disturbances at the cellular and mitochondrial level, mitochondrial electron transport chain complexes I–IV and apoptosis-inducing factor, and oxidative stress markers have been analyzed. Hydroxytyrosol improved the cardiac disturbances enhanced by doxorubicin by significantly reducing the percentage of altered mitochondria and oxidative damage. These results suggest that hydroxytyrosol improve the mitochondrial electron transport chain. This study demonstrates that hydroxytyrosol protect rat heart damage provoked by doxorubicin decreasing oxidative damage and mitochondrial alterations.ca_ES
dc.description.sponsorshipWe acknowledge grants from Excelentísima Diputación de Jaén, CEAS Foundation30.C0.244500 and Junta de AndalucíaPI-0210/2007. We thank the Spanish Ministry of Science and Innovation (AP2005-144) and the University of Granada for the personal support of Dr. S. Granados-Principal. Work carried out at the Department of Experimental Medicine was supported in part by R + D grants from the Spanish Ministry of Science and Innovation (BFU2009-11879/BFI), the Spanish Ministry of Health [RD06/0013/0012 and PI081843], the Autonomous Government of Catalonia [2009SGR735] and COST B35 Action of the European Union. We thank Dr. Elvin Blanco for help in editing of the final manuscript.ca_ES
dc.language.isoengca_ES
dc.publisherElsevierca_ES
dc.relationMICINN/PN2008-2011/BFU2009-11879/BFI
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1016/j.bcp.2014.04.001ca_ES
dc.relation.ispartofBiochemical Pharmacology , 2014, vol. 90, núm. 9, p. 25-33ca_ES
dc.rights(c) Elsevier, 2014ca_ES
dc.subjectOxidative stressca_ES
dc.subjectApoptosis-inducing factorca_ES
dc.subjectElectron transport chainca_ES
dc.subjectProtein damageca_ES
dc.titleHydroxytyrosol ameliorates oxidative stress and mitochondrial dysfunction in doxorubicin-induced cardiotoxicity in rats with breast cancerca_ES
dc.typearticleca_ES
dc.identifier.idgrec021861
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.1016/j.bcp.2014.04.001
dc.date.embargoEndDate2025-01-01


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