RESUMO
Anabolic androgenic steroids [AAS] are synthetic analogues of the natural androgenic male hormone called testosterone that is produced primarily in the testes in males and in the ovaries in females. Anabolic steroids are effective in enhancing athletic performance, in an effort to deliver a more optimal protein tissue building [anabolic] effect with less of the potential for musculinizing [androgenic] side-effects that are characteristic of testosterone itself. To shed light on the possible role of anabolic steroids in the induction of cardiac lesions; and experimental study as conducted on 30 male Wister rats divided into three groups, 10 per each group. The group 1 served as a control, group II [Nandorlene decanoate group] received 1 mg. [deca-durabolin[registered sign] 2.5 mg] by IM injection once daily for 14 consecutive days. Lastly, the group III [trimetazidine group] received Deca-durabolin in the same previous described regimen plus [Vastarel [registered sign] intraperitoneally in a dose f 5mg/kg dissolved in saline. All groups were scarified by decapitation on the 15[th] day. The supratherapeutic dose of AAS used in this study was chosen to mimic the self administered heavy abuse of AAS taken by body-builders. To assess cardiotoxicity, blood samples were collected for analysis of serum LDH, CPK-MB, and cardia content of catalase, and reduced glutathione and expression of caspase 3 protein [one of the antiapoptotic markers]. The cardiac muscle was separated and excised for immunohistochemistry and slot blot of caspase 3 and H and E examination. The Nandorlene decanoate group showed a highly significant elevated serum LDH and CPK-MB levels, and a highly significant depletion in cardia catalase, and reduced glutathione. The trimetazidine group showed a highly significant reduced serum LDH and CPK-MB, with a highly significant increased cardia catalase and reduced glutathione. Immunohistochemical cardiac examination of caspase 3 protein of the Nandorlene decanoate group showed increased expression which is reduced after trimetazidine therapy as a protective drug. In addition, H and E study findings of group II [Nandorlene decanoate group] were corrected in group III after Trimetazidine therapy. These results confirm the cardiotoxic effects of anabolic steroid abuse and the alleviating effects after Trimetazidine use