Looking for Organ Damages Due to Anabolic-androgenic Steroids (AAS): Is Oxidative Stress the Culprit?

The aim of this review is to discuss the evidence on the potential role of oxidative stress in the mechanisms of AAS-induced toxicity. The adverse effects of chronic consumption of supraphysiological doses of AAS include endocrine, behavioral, hepatic, renal and cardiovascular abnormalities; this is of considerable importance because of the wellknown AAS abuse by adolescent bodybuilders and athletes and the emergence of adverse side effects including a number of cardiac and cardiovascular complications leading eventually to death in some cases. Accumulating evidence indicate that abuse of AAS may cause cardiovascular adverse side-effects including elevated blood pressure, alteration of the structure of the heart, congestive heart failure, stroke, sudden cardiac death and endothelial dysfunction. Under normal physiological conditions a major source of ROS in liver is mitochondria, additional sources in generating ROS are peroxisomes, xanthine oxidase, NADPH oxidase, acyl-CoA oxidase and cytochrome P-450. Poor information are available on the effects of AAS treatment on hepatic antioxidant capacity. Evidence of side effects affecting kidney and the renal function are sporadically emerging from clinical reports of renal disorders among AASs users, especially with elevated and prolonged use. Experimental evidence suggests that both nandrolone administration and strenuous exercise increase the extent of renal damage in response to renal toxic injury. From the data presented, we can realize that to date considerable research has led to the identification of a growing number of AAS-adverse effects due to abuse of these substances.