Document Detail

Molecular basis of anthracycline-induced cardiotoxicity and its prevention.
MedLine Citation:
PMID:  11001837     Owner:  NLM     Status:  MEDLINE    
Anthracyclines are a class of highly potent antitumor antibiotics utilized against hematologic and solid tumors in children and in adults. Their use has been limited primarily by their cardiotoxic side effects, which may lead to congestive heart failure. Although there is a linear relationship between the cumulative dose received and the incidence of cardiotoxicity, in some patients cardiotoxicity may develop at doses below the generally accepted threshold level. Anthracycline-induced cardiotoxicity is believed to be related to the generation of highly reactive oxygen species, which, by means of membrane lipid peroxidation, cause direct damage to cardiac myocyte membranes. Another important factor may be the relatively poor antioxidant defense system of the heart. In an attempt to circumvent these toxic effects, a wide variety of antioxidants have been used in cell culture, animal, and human studies without consistent beneficial effects. Moreover, none of the agents used to date are designed to act selectively upon the heart. If the cardiac complications resulting from anthracyclines could be reduced and/or prevented, higher doses could potentially be used, thereby increasing cancer cure rates. Furthermore, the incidence of cardiac toxicity resulting in congestive heart failure or even heart transplantation would be reduced, therefore increasing the quality and extent of life for cancer survivors. This article will review the basic science of free radical biology, the biology of oxygen-derived free radicals and antioxidant proteins, and explore some new and innovative approaches to limiting and/or preventing anthracycline-induced cardiotoxicity.
M S Horenstein; R S Vander Heide; T J L'Ecuyer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Molecular genetics and metabolism     Volume:  71     ISSN:  1096-7192     ISO Abbreviation:  Mol. Genet. Metab.     Publication Date:    2000 Sep-Oct
Date Detail:
Created Date:  2000-11-13     Completed Date:  2000-11-13     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9805456     Medline TA:  Mol Genet Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  436-44     Citation Subset:  IM    
Copyright Information:
Copyright 2000 Academic Press.
Division of Pediatric Cardiology, Children's Hospital of Michigan and Wayne State University, Detroit, Michigan 48201, USA.
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MeSH Terms
Anthracyclines / toxicity*
Antioxidants / metabolism,  therapeutic use
Cell Membrane / drug effects,  metabolism
Free Radicals / metabolism
Heart / drug effects*
Heart Failure / chemically induced,  prevention & control
Lipid Peroxidation
Oxidative Stress
Reg. No./Substance:
0/Anthracyclines; 0/Antioxidants; 0/Free Radicals

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