Effects of prolonged stanozolol treatment on antioxidant enzyme activities, oxidative stress markers, and heat shock protein HSP72 levels in rat liver.
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.
Pey
Angel
A
Department of Biochemistry and Molecular Biology I, Faculty of Chemistry, Complutense University, 28040 Madrid, Spain.
Saborido
Ana
A
Blázquez
Isabel
I
Delgado
Jerónimo
J
Megías
Alicia
A
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D015415:Biomarkers / Q000032:analysis; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D002374:Catalase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism*; D008099:Liver / Q000033:anatomy & histology / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D009929:Organ Size / Q000187:drug effects / Q000502:physiology; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D010805:Physical Conditioning, Animal; D051381:Rats; D017208:Rats, Wistar; D013197:Stanozolol / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000975:Antioxidants; D015415:Biomarkers; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D017392:Thiobarbituric Acid Reactive Substances; D013197:Stanozolol; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione