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

被引:24
作者
Chaves, Elen A. [1 ,2 ,3 ,4 ]
Fortunato, Rodrigo S. [2 ]
Carvalho, Denise P. [2 ]
Nascimento, Jose Hamilton M. [1 ]
Oliveira, Marcus F. [3 ,4 ]
机构
[1] Univ Fed Rio de Janeiro, Lab Eletrofisiol Cardiaca Antonio Paes de Carvalh, Inst Biofis Carlos Chagas Filho, BR-21941590 Rio De Janeiro, RJ, Brazil
[2] Univ Fed Rio de Janeiro, Lab Fisiol Endocrina Doris Rosenthal, Inst Biofis Carlos Chagas Filho, BR-21941590 Rio De Janeiro, RJ, Brazil
[3] Univ Fed Rio de Janeiro, Lab Bioquim Resposta Ao Estresse, Inst Bioquim Med, Programa Biol Mol & Biotecnol, BR-21941590 Rio De Janeiro, RJ, Brazil
[4] Univ Fed Rio de Janeiro, Lab Inflamacao & Metab, Inst Nacl Ciencia & Tecnol Biol Estrutural Bioima, BR-21941590 Rio De Janeiro, RJ, Brazil
关键词
Free radicals; Antioxidant; Reactive oxygen species; Metabolism; SUPEROXIDE-DISMUTASE; ISCHEMIA-REPERFUSION; MYOCARDIAL TOLERANCE; NANDROLONE; OXYGEN; TRANSCRIPTION; PROTEINS; STRESS; ABUSE;
D O I
10.1016/j.jsbmb.2013.06.006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:267 / 272
页数:6
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