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Updated: Mar 28, 2026
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Protective effects of mito-TEMPO against doxorubicin cardiotoxicity in mice
Viviane Costa Junqueira Rocha1, Luciana Souza de Aragão França1, Cintia Figueiredo de Araújo1
1Gonçallo Moniz Research Center, Fundação Oswaldo Cruz, Rua Waldemar Falcão 121, Salvador, BA, 40296-710, Brazil.
Purpose:
Doxorubicin (DOX) is a chemotherapeutic that is widely used for the treatment of many human tumors. However, the development of cardiotoxicity has limited its use. The aim of the present study was to evaluate the possible efficacy of mito-TEMPO (mito-T) as a protective agent against DOX-induced cardiotoxicity in mice.
Methods:
C57BL/6 mice were treated twice with mito-T at low (5 mg/kg body weight) or high (20 mg/kg body weight) dose and once with DOX (24 mg/kg body weight) or saline (0.1 mL/20 g body weight) by means of intraperitoneal injections. The levels of malondialdehyde (MLDA), a marker of lipid peroxidation, and serum levels of creatine kinase were evaluated 48 h after the injection of DOX.
Results:
DOX induced lipid peroxidation in heart mitochondria (p < 0.001), and DOX-treated mice receiving mito-T at low dose had levels of MLDA significantly lower than the mice that received only DOX (p < 0.01). Furthermore, administration of mito-T alone did not cause any significant changes from control values. Additionally, DOX-treated mice treated with mito-T at high dose showed decrease in serum levels of total CK compared to mice treated with DOX alone (p < 0.05).
Conclusion:
Our results indicate that mito-T protects mice against DOX-induced cardiotoxicity.
