ABSTRACT
The abuse of anabolic-androgenic steroids (AAS) to enhance physical performance is widespread in sport communities despite their reported side effects. Since the biochemical bases for the hepatotoxic effects of these compounds are largely unknown, this investigation was aimed at testing whether prolonged (8 weeks) treatment with high doses (2 mg kg(-1) body weight; 5 d wk(-1)) of stanozolol (ST), either alone or in conjunction with treadmill-exercise training, induced changes in oxidative stress biomarker levels and antioxidant defence systems in rat liver. After ST oral administration, the mean values of serum parameters related to hepatic function were within normal ranges. No changes in protein carbonyl content and in the reduced to oxidized glutathione (GSH/GSSG) ratio were detected in liver homogenates of ST-treated rats, whereas thiobarbituric acid-reactive substances (TBARS) levels resulted increased (P<0.05). Total superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities were higher (P<0.05) in the liver of treated rats but mitochondrial SOD and glutathione reductase (GR) activities, and the 72 kDa heat shock protein (HSP72) level were not modified. Chronic exercise alone did not change any of the above parameters except for a remarkable enhancement of HSP72 expression; in no case training modified the effects of ST treatment. The present data show that 8 wk ingestion of ST, either with or without concurrent exercise training, can induce oxidative stress in rat liver despite the up-regulation of enzymatic antioxidant activities.
Subject(s)
Antioxidants/metabolism , Heat-Shock Proteins/metabolism , Liver/drug effects , Liver/metabolism , Stanozolol/pharmacology , Animals , Biomarkers/analysis , Body Weight/drug effects , Body Weight/physiology , Catalase/metabolism , Glutathione/metabolism , Glutathione Peroxidase/metabolism , HSP72 Heat-Shock Proteins , Liver/anatomy & histology , Liver/enzymology , Male , Organ Size/drug effects , Organ Size/physiology , Oxidation-Reduction , Oxidative Stress/physiology , Physical Conditioning, Animal , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/metabolismABSTRACT
The purpose of this work was to study whether exercise training induces changes in the lipid profile of rat aorta and nervous system and in the in vitro intrinsic responsiveness of these tissues to endothel in-1 (ET-1) treatment. The exercise program performed successfully produced the characteristic metabolic alterations of the trained state. Exercise training induced a large and significant increase in the levels of both aortic ethanolamine plasmalogens (PlasEtn) and glucosylceramides. In contrast, a decrease of aortic ceramide and cholesterol levels was evoked by exercise training. ET-1 increased PlasEtn content only in sedentary animals. An exercise-induced increase in cerebellum levels of ceramides and ceramide monohexosides was found. The cerebellum ceramide content was increased by ET-1 more noticeably in sedentary rats than in trained animals. In contrast, cerebral cortex was observed to be largely insensitive to both exercise training and ET-1 treatment. It was concluded that exercise training (i) induces changes in both vascular and cerebellar lipid profiles, the former being much more pronounced than the latter, and (ii) diminishes the aortic and cerebellar sensitivity to ET-1 action.
