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Cardiac Toxicity of Anthracyclines

Target Organ and Tissue Toxicity

  1. Richard D. Olson PhD1,2,3,
  2. Barry J. Cusack MD1,2,3,4

Published Online: 15 DEC 2009

DOI: 10.1002/9780470744307.gat177

General, Applied and Systems Toxicology

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. .

Author Information

  1. 1

    Veterans Affairs Medical Center, Captain Marshall Woods Research Service, Boise, Idaho, USA

  2. 2

    Mountain States Tumor and Medical Research Institute, St. Luke's Regional Medical Center, Boise, Idaho, USA

  3. 3

    University of Washington School of Medicine, Department of Medicine, Seattle, Washington, USA

  4. 4

    St. Luke's Regional Medical Center, Mountain States Tumour and Medical Research Institute, Boise, Idaho, USA

Publication History

  1. 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.


  • anthracyclines;
  • cardiotoxicity;
  • heart failure;
  • calcium;
  • free radicals;
  • ageing