Cardiac Toxicity of Anthracyclines
Target Organ and Tissue Toxicity
Published Online: 15 DEC 2009
Copyright © 2009 John Wiley & Sons, Ltd. All rights reserved.
General, Applied and Systems Toxicology
How to Cite
Olson, R. D. and Cusack, B. J. 2009. Cardiac Toxicity of Anthracyclines. General, Applied and Systems Toxicology. .
- Published Online: 15 DEC 2009
Cardiotoxicity of anthracyclines limits their therapeutic potential. In the in vitro acute model, anthracyclines produce cardiotoxicity in minutes or hours at concentrations near 100 μM, through a mechanism involving impairment of sarcoplasmic reticulum (SR) function and requiring the quinone moiety, most likely through a non-free-radical process. The chronic cardiotoxicity is more complex, but may also involve SR. Additional mechanisms in the chronic model of anthracycline cardiotoxicity may include impairment of triiodothyronine function, cardiac protein degradation, free-radical generation, apoptosis, cardiac metabolite formation, impairment of iron metabolism and oestrogen-dependent up-regulation of nitric oxide synthase (NOS). Thus, prevention or attenuation of anthracycline cardiotoxicity may be achieved by favourably manipulating these mechanisms.
- heart failure;
- free radicals;