Rat liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids. Med. Sci. Sports Exerc., Vol. 31, No. 2, pp. 243-250, 1999.
The aim of this study was to examine the separate and combined effects of an 8-wk treatment with high doses of 17α-alkylated anabolic-androgenic steroids (AAS) and exercise training on selected lysosomal and mitochondrial enzyme activities in rat liver.
Sedentary and treadmill-trained (25 m·min−1, 45 min·d−1, 5 d·wk−1) male rats were treated with fluoxymesterone, methylandrostanolone, or stanozolol (2 mg·kg body weight−1, 5 d·wk−1) for 8 wk.
Acid phosphatase, arylsulfatase, β-glucuronidase, and β-galactosidase activities were increased in liver homogenates of sedentary and trained AAS-treated rats. The mitochondrial respiratory chain activities rotenone-sensitive NADH-cytochrome c reductase (NCCR), succinate cytochrome c reductase (SCCR), and cytochrome oxidase (COX) showed a significant decrease in steroid-administered rats, whereas citrate synthase (CS), a matrix enzyme, exhibited no changes in activity, pointing to a selective effect of AAS on mitochondrial membrane complexes. In vitro studies in mitochondrial fractions isolated from the liver of control rats showed that COX and CS activities were insensitive to the AAS, whereas NCCR and SCCR activities were partly inhibited. On the other hand, the mean values of serum parameters related to hepatic function were within normal ranges in all the experimental groups of animals.
The present data show that 8-wk ingestion of three different anabolic-androgenic steroids, either with or without concurrent exercise training, affects lysosomal hydrolases and mitochondrial respiratory chain electron transport in rat liver without modifying classical serum indicators of hepatic function.
Department of Biochemistry and Molecular Biology I, Faculties of Chemistry and Biology, Complutense University, Madrid, SPAIN
Submitted for publication July 1997.
Accepted for publication May 1998.
We thank Zambon S. A. (Barcelona, Spain) for the gift of stanozolol. This work was supported by grants SAF93-0287 from the CICYT and PM95-0190 from the DIGICYT (Spain).
Address for correspondence: Dra. Alicia Megías, Dpto. Bioquímica y Biología Molecular I, Facultad de Biología, Universidad Complutense, 28040-Madrid, Spain. E-mail: email@example.com.