The induction of CYP1A by the polycyclic aromatic hydrocarbon (PAH)-type inducer β-naphthoflavone (BNF) in the Poeciliopsis-lucida hepatocellular carcinoma cell line (PLHC-1), and the effects of the glucocorticoid receptor (GR) agonist dexamethasone (DEX) on this response were examined. Dose-response studies revealed that BNF is three orders of magnitude less potent than the planar halogenated aromatic hydrocarbon 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as an inducer of the CYP1A activity ethoxyresorufin-O-deethylase (EROD), and that the apparent efficacy for the induction by BNF is 50% of that obtained with TCDD. Addition of 10 μM DEX resulted in potentiation of CYP1A induction at all doses of BNF tested. The degree of that potentiation of induction of CYP1A protein levels and EROD activity differed substantially between doses of BNF and at different times of exposure. For example, the maximal degree of potentiation of EROD induction by DEX was 12-fold in PLHC-1 cells treated with 0.1 μM BNF, 19-fold in cells treated with 1 μM BNF, and 8-fold in cells treated with 10 μM BNF. These maximal degrees of potentiation of EROD induction were obtained after 30 h with 0.1 μM BNF, 48 h with 1 μM BNF, and 72 h with 10 μM BNF. These results demonstrate interactions between GR and aryl hydrocarbon receptor pathways that could influence the response of fish to xenobiotic exposure.