Effects of Chronic Exposure to PCBs on Cytochrome P450 Systems and Steroidogenesis in Liver and Testis of Bulls (Bos Taurus)

Effects of chronic exposure to PCBs on the microsomal cytochrome P450 (CYP) enzymes in liver and testis of bulls (Bos taurus) were determined by comparing the constitutive and PCB-induced alkoxyresorufin O-dealkylase and testosterone hydroxylase activities. Specific inductions of the prevailing hepatic ethoxyresorufin O-deethylation and 6 beta-hydroxylation of testosterone are suggestive of the induction of CYP1A1 and CYP3A-like enzymes by PCBs. A high level of PCB-inducible androstenedione formation was also found. The hepatic CYP2B activities (i.e. pentoxyresorufin O-depentylase and testosterone 16 beta-hydroxylase) and CYP2C11-like testosterone 2 alpha-hydroxylase were increased only weakly. The testicular microsomal CYP activities were non-specifically reduced by the PCB exposure, except for the androstenedione formation and 16 beta-hydroxylation of testosterone. The inhibition of the activity of mitochondrial CYP11A, as the rate-limiting enzyme of steroidogenesis measured with resorufin 3 beta-hydroxy-22,23-bisnor-5-cholenyl ether as the fluorogenic substrate, exceeded 50% in testes of the PCB-contaminated bulls. The latter activity as well as the hepatic testosterone 6 beta-hydroxylation and hepatic and testicular androstenedione formation may significantly contribute to the decrease in testosterone levels after the PCB intake.