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Updated: May 10, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Exercise-induced cardioprotection is impaired by anabolic steroid treatment through a redox-dependent mechanism
Elen A Chaves1, Rodrigo S Fortunato, Denise P Carvalho
1Laboratório de Eletrofisiologia Cardíaca Antonio Paes de Carvalho, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Brazil; Laboratório de Fisiologia Endócrina Doris Rosenthal, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Brazil; Laboratório de Bioquímica de Resposta ao Estresse, Instituto de Bioquímica Médica, Programa de Biologia Molecular e Biotecnologia, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Brazil; Laboratório de Inflamação e Metabolismo, Instituto Nacional de Ciência e Tecnologia de Biologia Estrutural e Bioimagem (INBEB), Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Abstract:
High doses of anabolic androgenic steroids (AAS) impair the cardioprotective effects of exercise against ischemia/reperfusion (I/R) insult, possibly through cellular redox imbalance. Here, the effect of nandrolone decanoate (DECA) treatment on heart redox metabolism was investigated during I/R in sedentary and exercised rats. DECA treatment significantly reduced superoxide dismutase and glutathione reductase activities in exercised rats after heart reperfusion. Catalase and glutathione peroxidase activities were not affected by DECA in both sedentary and trained rats, regardless the I/R period. DECA also induced myocardial oxidative stress, as evidenced by the reduced levels of total reduced thiols after heart reperfusion in exercised rats treated with the anabolic steroid. These results indicate that cardiotoxic effects of supraphysiological doses of AAS involve reduced heart antioxidant capacity.
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