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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/70604
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dc.contributor.authorFerreira, Ana Lúcia dos Anjos-
dc.contributor.authorMatsubara, Luiz Shiguero-
dc.contributor.authorMatsubara, Beatriz Bojikian-
dc.date.accessioned2014-05-27T11:23:41Z-
dc.date.accessioned2016-10-25T18:26:03Z-
dc.date.available2014-05-27T11:23:41Z-
dc.date.available2016-10-25T18:26:03Z-
dc.date.issued2008-10-01-
dc.identifierhttp://dx.doi.org/10.2174/187152508785909474-
dc.identifier.citationCardiovascular and Hematological Agents in Medicinal Chemistry, v. 6, n. 4, p. 278-281, 2008.-
dc.identifier.issn1871-5257-
dc.identifier.urihttp://hdl.handle.net/11449/70604-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/70604-
dc.description.abstractThe anthracyclines constitute a group of drugs widely used for the treatment of a variety of human tumors. However, the development of irreversible cardiotoxicity has limited their use. Anthracycline-induced cardiotoxicity can persist for years with no clinical symptoms. However, its prognosis becomes poor after the development of overt heart failure, possibly even worse than ischemic or idiopathic dilated cardiomyopathies. Due to the successful action of anthracyclines as chemotherapic agents, several strategies have been tried to prevent/ attenuate their side effects. Although anthracycline-induced injury appears to be multifactorial, a common denominator among most of the proposed mechanisms is cellular damage mediated by reactive oxygen species. However, it remains controversial as to whether antioxidants can prevent such side effects given that different mechanisms may be involved in acute versus chronic toxicity. The present review applies a multisided approach to the critical evaluation of various hypotheses proposed over the last decade on the role of oxidative stress in cardiotoxicity induced by doxorubicin, the most used anthracycline agent. The clinical diagnosis and treatment is also discussed. © 2008 Bentham Science Publishers Ltd.en
dc.format.extent278-281-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectCardiomyopathy-
dc.subjectDNA damage-
dc.subjectDoxorubicin-
dc.subjectFree radicals-
dc.subjectOxidative stress-
dc.subjectReactive Oxygen Species-
dc.subjectalpha tocopherol-
dc.subjectamifostine-
dc.subjectanthracycline derivative-
dc.subjectantioxidant-
dc.subjectascorbic acid-
dc.subjectbeta adrenergic receptor blocking agent-
dc.subjectbeta carotene-
dc.subjectcannabinoid 1 receptor-
dc.subjectcannabinoid 1 receptor antagonist-
dc.subjectcyclophosphamide-
dc.subjectcytarabine-
dc.subjectdigoxin-
dc.subjectdipeptidyl carboxypeptidase inhibitor-
dc.subjectDNA topoisomerase (ATP hydrolysing)-
dc.subjectdoxorubicin-
dc.subjectflavonoid-
dc.subjectglutathione-
dc.subjectidarubicin-
dc.subjectinducible nitric oxide synthase-
dc.subjectlycopene-
dc.subjectolive oil-
dc.subjectpolyphenol derivative-
dc.subjectprobucol-
dc.subjectrazoxane-
dc.subjectreactive nitrogen species-
dc.subjectreactive oxygen metabolite-
dc.subjectretinol-
dc.subjectselenium-
dc.subjectubiquinone-
dc.subjectunindexed drug-
dc.subjectantioxidant activity-
dc.subjectaspartate aminotransferase blood level-
dc.subjectcardiomyopathy-
dc.subjectcardiotoxicity-
dc.subjectcardiovascular risk-
dc.subjectclinical feature-
dc.subjectcreatine kinase blood level-
dc.subjectdiagnostic value-
dc.subjectdose response-
dc.subjectdrug dose reduction-
dc.subjectdrug efficacy-
dc.subjectdrug induced disease-
dc.subjectdrug safety-
dc.subjectdrug withdrawal-
dc.subjectearly diagnosis-
dc.subjectECG abnormality-
dc.subjectechocardiography-
dc.subjectelectrocardiography-
dc.subjectfollow up-
dc.subjecthealth care cost-
dc.subjectheart arrhythmia-
dc.subjectheart failure-
dc.subjectheart muscle biopsy-
dc.subjectheart protection-
dc.subjectheart transplantation-
dc.subjecthuman-
dc.subjecthypotension-
dc.subjectincidence-
dc.subjectlactate dehydrogenase blood level-
dc.subjectneoplasm-
dc.subjectnonhuman-
dc.subjectoxidative stress-
dc.subjectpathogenesis-
dc.subjectprimary prevention-
dc.subjectprognosis-
dc.subjectprotein expression-
dc.subjectQRS complex-
dc.subjectQT prolongation-
dc.subjectreview-
dc.subjectrisk factor-
dc.subjectside effect-
dc.subjectsingle drug dose-
dc.subjectST segment-
dc.subjecttachycardia-
dc.subjectAnimals-
dc.subjectAntibiotics, Antineoplastic-
dc.subjectCalcium-
dc.subjectDNA Damage-
dc.subjectElectrocardiography-
dc.subjectHeart-
dc.subjectHumans-
dc.subjectOxidative Stress-
dc.titleAnthracycline-induced cardiotoxicityen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationDepartment of Internal Medicine Botucatu Medical School UNESP - São Paulo State University, 18618-970 Botucatu, SP-
dc.description.affiliationUnespDepartment of Internal Medicine Botucatu Medical School UNESP - São Paulo State University, 18618-970 Botucatu, SP-
dc.identifier.doi10.2174/187152508785909474-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofCardiovascular and Hematological Agents in Medicinal Chemistry-
dc.identifier.scopus2-s2.0-54949128285-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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