Exercise-induced cardioprotection is impaired by anabolic steroid treatment through a redox-dependent mechanism

• Published in: The Journal of steroid biochemistry and molecular biology Vol. 138; pp. 267 - 272
• Main Authors: Chaves, Elen A., Fortunato, Rodrigo S., Carvalho, Denise P., Nascimento, José Hamilton M., Oliveira, Marcus F.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.11.2013
• Subjects: Anabolic Agents - adverse effects; Animals; Antioxidant; Dequalinium - analogs & derivatives; Dequalinium - pharmacology; Free radicals; Glutathione Reductase - metabolism; Heart - drug effects; Heart - physiology; Male; Metabolism; Oxidation-Reduction - drug effects; Oxidative Stress - drug effects; Physical Conditioning, Animal - physiology; Rats; Rats, Wistar; Reactive oxygen species; Superoxide Dismutase - metabolism; Reactive oxygen species; Free radicals; Antioxidant; Metabolism
• ISSN: 0960-0760; 1879-1220
• DOI: 10.1016/j.jsbmb.2013.06.006

•Supraphysiological DECA treatment on heart redox metabolism was investigated during I/R in sedentary and exercised rats.•DECA reduced SOD and GR activities in exercised rats upon reperfusion.•Reduced antioxidant enzyme activities promote heart thiol oxidation in exercised rats.•Anabolic androgenic steroid abuse cardiotoxicity involves redox imbalance in exercised animals. 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.