Anabolic Steroid - and Exercise - Induced Cardio-Depressant Cytokines and Myocardial β1 Receptor Expression in CD1 Mice

Author(s): Irene Riezzo, Marco Di Paolo, Margherita Neri, Stefania Bello, Santina Cantatore, Stefano D'Errico, Dinuccio Dinucci, Ruggero Parente, Cristoforo Pomara, Roberto Rabozzi, Emanuela Turillazzi, Vittorio Fineschi.

Journal Name: Current Pharmaceutical Biotechnology

Volume 12 , Issue 2 , 2011

Become EABM
Become Reviewer


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 β1 adrenergic receptor expression, and the effects of the myocardial expression of inflammatory mediators (IL-1β, TNF-α) on the induction of cardiomyocytes apoptosis (HSP70, 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.

Keywords: AAS toxicity, apoptosis, 1 adrenergic receptor, cardiac damage, cytokines, interleukins

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2011
Page: [275 - 284]
Pages: 10
DOI: 10.2174/138920111794295792
Price: $65

Article Metrics

PDF: 22