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Lab Anim Res. 2017 Jun;33(2):165-170. doi: 10.5625/lar.2017.33.2.165. Epub 2017 Jun 30.

Comparision of doxorubicin-induced cardiotoxicity in the ICR mice of different sources.

Author information

1
College of Pharmacy, Pusan National University, Busan, Korea.
2
Department of Biomedical Laboratory Science, Daekyeung College, Gyeongsan, Korea.
3
College of Pharmacy, Kyungsung University, Busan, Korea.
4
Department of Microbiology and Immunology, INJE University College of Medicine, Busan, Korea.
5
Exercise Biochemistry Laboratory, Korea National Sport University, Seoul, Korea.
6
Department of Biomaterials Science, College of Natural Resources & Life Science/Life and Industry Convergence Research Institute, Pusan National University, Miryang, Korea.
7
College of Veterinary Medicine, Kyungpook National University, Daegu, Korea.

Abstract

Doxorubicin is a widely used chemotherapeutic agents and is now part of standard therapeutic regimens for a variety of cancers (eg, hematopoietic malignancies and advanced solid tumors of the breast, ovary, thyroid, and bone). However, a potentially lethal and dose-dependent cardiotoxicity that appears within a short time after treatment limits the usage of doxorubicin in cancer patients. Although the mechanism of doxorubicin-induced cardiotoxicity is not completely understood, it is thought that free radical-induced oxidative stress and excessive production of reactive oxygen species are primary drivers of its toxicity. In this study, we compared the doxorubicin-induced cardiotoxicity of ICR mice obtained from three different sources and evaluated the utility of Korl:ICR stock established by the Korean FDA. Because doxorubicin-induced cardiotoxicity is thought to involve the excessive generation of ROS followed by oxidative stress, we determined the representative tissue index of oxidation, lipid peroxidation, and antioxidant, glutathione (GSH), as well as the parameters of heart injury. Doxorubicin treatment successfully induced cardiotoxicity as evidenced by histological examination and serum parameters (eg, levels of LDH and CK activities) in ICR mice. It was accompanied by increased lipid peroxidation and a decrease in both cysteine and GSH, further supporting previous reports that oxidative stress is a potential mechanism of doxorubicin-induced cardiotoxicity. Of interest, we did not observe a significant difference in doxorubicin-induced cardiotoxicity among mice of different origins. Collectively, our results suggest that Korl:ICR strain may be useful in the research of doxorubicin-induced cardiotoxicity.

KEYWORDS:

Cardiotoxicity; ICR mouse; doxorubicin; oxidative stress

Conflict of interest statement

Conflict of interests: The authors declare that there is no financial conflict of interests to publish these results.

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