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.