Teleosts are exposed, in the environment, to a number of chemicals that are capable of inducing hepatic cytochrome P450 monooxygenase activity. This induction has been described as a most sensitive biological indicator of the presence of certain classes of chemicals in water. The concept of a bioindicator, as applied here, is derived from the idea that a toxic effect will be manifested at the subcellular level before effects will be apparent at higher levels of biological organization. Laboratory and environmental induction of hepatic cytochrome P450 CYP1A1 (P450IA1) was investigated using catalytic activity, immunodetection and nucleic acid hybridization. Rainbow trout and largemouth bass were exposed, underflow-through conditions, to beta-naphthoflavone (beta-NF), a known CYP1A1 inducer, at concentrations ranging from 0-625 to 500 mug beta-NF/liter for periods of 1 to 21 days. At concentrations of 50-500 mug beta-NF/liter, ethoxyresorufin-O-deethylase (EROD) activity and immunoreactive CYP1A1 levels were induced, but the induction was inversely related to the beta-NF concentration. At these same concentrations, hybridizable CYP1A1 mRNA was increased at all concentrations over time and was induced at least up to 7 days of beta-NF treatment. At concentrations of 0.625-10.0 mug beta-NF/liter, EROD activity, immunoreactive protein and hybridizable mRNA were increased in a concentration-dependent manner. Environmental exposure of largemouth bass, placed in cages in water known to be contaminated with polychlorinated biphenyls, had elevated (six-fold) EROD activity at 3 and 7 days. Killifish taken from a TCDD-contaminated site had three-fold higher EROD activity and CYP1A1 mRNA, as well as increased immunoreactive protein, than killifish from a 'clean' site. These data indicate the efficacy of using nucleic acid hybridization of CYP1A1 mRNA as a bioindicator of environmental contamination.