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Oxidative Medicine and Cellular Longevity
Volume 2012, Article ID 681367, 9 pages
Research Article

The Redox Imbalance and the Reduction of Contractile Protein Content in Rat Hearts Administered with L-Thyroxine and Doxorubicin

1Medical Biology Unit, Medical University of Lublin, 20-950 Lublin, Poland
2Human Anatomy Department, Medical University of Lublin, 20-950 Lublin, Poland
3Clinical Pathomorphology Department, Medical University of Lublin, 20-950 Lublin, Poland
4Oncological Pneumology and Alergology Department, Medical University of Lublin, 20-950 Lublin, Poland
5Lloyds Pharmacy, 333 Meadowhead, Sheffield S8 9TU, UK

Received 7 August 2011; Revised 15 October 2011; Accepted 15 November 2011

Academic Editor: Neelam Khaper

Copyright © 2012 Agnieszka Korga et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Oxidative stress and disorders in calcium balance play a crucial role in the doxorubicin-induced cardiotoxicity. Moreover, many cardiotoxic targets of doxorubicin are regulated by iodothyronine hormones. The aim of the study was to evaluate effects of tetraiodothyronine (0.2, 2 mg/L) on oxidative stress in the cardiac muscle as well as contractility and cardiomyocyte damage markers in rats receiving doxorubicin (1.5 mg/kg) once a week for ten weeks. Doxorubicin was administered alone (DOX) or together with a lower (0.2T4 + DOX) and higher dose of tetraiodothyronine (2T4 + DOX). Two groups received only tetraiodothyronine (0.2T4, 2T4). Coadministration of tetraiodothyronine and doxorubicin increased the level of lipid peroxidation products and reduced RyR2 level when compared to untreated control and group exposed exclusively to doxorubicin. Insignificant differences in SERCA2 and occasional histological changes were observed. In conclusion, an increase of tetraiodothyronine level may be an additional risk factor of redox imbalance and RyR2 reduction in anthracycline cardiotoxicity.