Anabolic steroid- and exercise-induced cardio-depressant cytokines and myocardial β1 receptor expression in CD1 mice

Curr Pharm Biotechnol. 2011 Feb 1;12(2):275-84. doi: 10.2174/138920111794295792.


Few animal model studies have been conducted in order to evaluate the impact of androgenic anabolic steroids (AAS) supraphysiological doses on the cardiovascular system and myocardial injury. Twenty-five male CD1 mice (8-10 weeks old; 35g initial body weight) were randomized into three AAS treated groups and two control groups. The AAS mice received intramuscular Nandrolone Decanoate (DECA-DURABOLIN), vehicled in arachidis oil, for 42 days, twice per week, with different dosages, studying plasma lipid analysis, cardiac histopathological features, cardiac β (1) adrenergic receptor expression, and the effects of the myocardial expression of inflammatory mediators (IL-1β, TNF-α) on the induction of cardiomyocytes apoptosis (HSP 70, TUNEL), using proteomic and immunohistochemical analysis. The mice had free movements in their animal rooms (two groups) or exercised by running on a motor-driven treadmill the others three groups. Recurring high dose AAS administration and physical training in mice produce significant increase in body weight and for total cholesterol. A moderate increase of the heart weight, cardiac hypertrophy and wide colliquative myocytolysis, were observed in high dose AAS administration and physical training group. The expression of HSP70 and inflammatory cytokine IL-1β, increased in the three AAS-treated groups. TNF- α showed a more extensive expression in the AAS-high dose group. A significant apoptotic process randomly sparse in the myocardium was described. Our data support the hypothesis that the combined effects of vigorous training, anabolic steroid abuse and stimulation of the sympathetic nervous system, may predispose to myocardial injury.

MeSH terms

  • Anabolic Agents / administration & dosage
  • Anabolic Agents / pharmacology*
  • Anabolic Agents / toxicity
  • Animals
  • Apoptosis / drug effects
  • Cytokines / biosynthesis*
  • Cytokines / metabolism
  • Heart / drug effects*
  • Heart / physiopathology
  • In Situ Nick-End Labeling
  • Lipids / blood
  • Male
  • Mice
  • Models, Animal
  • Myocardium / metabolism
  • Nandrolone / administration & dosage
  • Nandrolone / analogs & derivatives*
  • Nandrolone / pharmacology
  • Nandrolone / toxicity
  • Nandrolone Decanoate
  • Physical Conditioning, Animal*
  • Random Allocation
  • Receptors, Adrenergic, beta-1 / biosynthesis*
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / metabolism


  • Anabolic Agents
  • Cytokines
  • Lipids
  • Receptors, Adrenergic, beta-1
  • Tumor Necrosis Factor-alpha
  • Nandrolone
  • Nandrolone Decanoate