The aim of this study is to assess cardiotoxic effect of testosterone (TES) and dehydroepiandrosterone (DHEA) in Sprague Dawley rats. We compared the impact of subacute (14 days) and subchronic (90 days) administration of suprapharmacologic doses of TES and DHEA on body weight, locomotor activity, muscle strength, echocardiographic parameters, heart histopathology, and oxidative stress markers with the control group. Testosterone (10, 30, and 100 mg/100 g body weight) and DHEA (10 mg/100 g body weight) administration decreased the body weights and locomotor activity ( p < 0.05), and the combination of both increased muscle strength ( p < 0.05) in rats. In our histopathological evaluation, misshapen cell nuclei, disorganized myocardial fibers, and leukocytic infiltrates were observed in high-dose TES (100 mg/100 g)-treated rats, especially on day 14. On day 90, mild changes such as misshapen cell nuclei, disorganized myocardial fibers, and leukocytic infiltrates were observed in TES and DHEA-treated groups. According to our echocardiographic study on day 14 and day 90, TES, especially at high doses, induced increase in left ventricular posterior wall diameter and ejection fraction ( p < 0.05). In this study, blood oxidative stress marker malondialdehyde was increased slightly but not significantly in TES and DHEA groups. On the other hand, antioxidant enzymes such as SOD and glutathione peroxidase (GSH-Px) levels were slightly but not significantly increased in TES and DHEA groups. These data demonstrate that the potential risk to cardiac health due to exogenous androgen use may be related to oxidative stress in rats.
Anabolic Androjenic streoids (AAS) are synthetic derivatives of testosterone which promote growth of skeletal muscle (anabolic effect) and the development of the male sexual characteristics (androgenic effects). Illegally, these drugs are regulary self-administered by power lifters and bodybuilders to enhance their sportive performance. Abuse of AAS has been linked to a variety of different cardiovascular side effects. In case reports, acute myocardial infarction is the most common event presented, but other adverse side effects include left ventricular hypertrophy, reduced left ventricular contractile function, hypertension, arterial thrombosis, pulmonary embolism, endothelial dysfunction, alterations of lipid metabolism, life-threatening arrytmia and several cases of sudden cardiac death. However, to date, there are no prospective, randomized, interventional studies on the long term cardiovascular effects of abuse of AAS. In this review, we have tried to summarize recent literature and our recent observations in experimental animals related to AAS-induced cardiotoxicity. Additionally we will discuss possible mechanisms of this adverse effect.
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