Ferreira, Ana Lúcia dos Anjos [UNESP]Matsubara, Luiz Shiguero [UNESP]Matsubara, Beatriz Bojikian [UNESP]2014-05-272014-05-272008-10-01Cardiovascular and Hematological Agents in Medicinal Chemistry, v. 6, n. 4, p. 278-281, 2008.1871-5257http://hdl.handle.net/11449/70604The 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.278-281engCardiomyopathyDNA damageDoxorubicinFree radicalsOxidative stressReactive Oxygen Speciesalpha tocopherolamifostineanthracycline derivativeantioxidantascorbic acidbeta adrenergic receptor blocking agentbeta carotenecannabinoid 1 receptorcannabinoid 1 receptor antagonistcyclophosphamidecytarabinedigoxindipeptidyl carboxypeptidase inhibitorDNA topoisomerase (ATP hydrolysing)doxorubicinflavonoidglutathioneidarubicininducible nitric oxide synthaselycopeneolive oilpolyphenol derivativeprobucolrazoxanereactive nitrogen speciesreactive oxygen metaboliteretinolseleniumubiquinoneunindexed drugantioxidant activityaspartate aminotransferase blood levelcardiomyopathycardiotoxicitycardiovascular riskclinical featurecreatine kinase blood leveldiagnostic valuedose responsedrug dose reductiondrug efficacydrug induced diseasedrug safetydrug withdrawalearly diagnosisECG abnormalityechocardiographyelectrocardiographyfollow uphealth care costheart arrhythmiaheart failureheart muscle biopsyheart protectionheart transplantationhumanhypotensionincidencelactate dehydrogenase blood levelneoplasmnonhumanoxidative stresspathogenesisprimary preventionprognosisprotein expressionQRS complexQT prolongationreviewrisk factorside effectsingle drug doseST segmenttachycardiaAnimalsAntibiotics, AntineoplasticCalciumDNA DamageElectrocardiographyHeartHumansOxidative StressArtigo10.2174/187152508785909474Acesso restrito2-s2.0-54949128285294005165084654163098351379987666990977122340795