AIM: To study the effects of diphenytriazol on cytochrome P-450 (CYP) enzymes. METHODS: SD rats were pretreated with diphenytriazol. The catalytic activities of rat liver microsomes were determined by assaying ethoxyresorufin-O-deethylase (EROD) and pentoxyresorufin-O-dealkylase. Phenacetin and aminopyrine were se- lected as the substrate of CYP1A and CYP2B, respectively. The concentration of remaining substrate in microso- mal incubates was determined by reversed-phase high-performance liquid chromatography (RP-HPLC). The inhi- bition of fluvoxamine or α-naphthoflavone on phenacetin metabolism was measured. RESULTS: Phenacetin was significantly metabolized in the diphenytriazol-treated microsomes and the metabolic degree increased according to the diphenytriazol-treatment days. There existed a significant correlation between the metabolic degree of phenace- tin and EROD in the microsomes pretreated with diphenytriazol. Both fluvoxamine and α-naphthoflavone inhibited the metabolism of phenacetin significantly, and the inhibition constants (Ki) were (5.4±1.0) μmol/L and (10.4±0.5) μmol/L, respectively. The activity of microsomes pretreated with diphenytriazol for 4 d was similar to that in β- naphthoflavone group, but was significantly different from those in control group and phenobarbital group. CONCLUSION: These results reveal that diphenytriazol is a novel inducer of CYP1A. METHODS: SD rats were pretreated with diphenytriazol. The catalytic activities of rat liver microsomes determined by assaying ethoxyresorufin-O-deethylase (EROD) and pentoxyresorufin-O -dealkylase. Phenacetin and aminopyrine were selected as the substrate of CYP1A and CYP2B, respectively. The concentration of remaining substrate in microso-mal liquid samples was determined by RP-HPLC. The inhi- bition of fluvoxamine or α-naphthoflavone on phenacetin metabolism was measured. RESULTS: Phenacetin was significantly metabolized in the diphenytriazol-treated microsomes and the metabolic degree increased according to the diphenytriazol-treatment days. There existed a significant correlation between the metabolic degree of phenace- tin and EROD in the microsomes pretreated with diphenytriazol. Both fluvoxamine and α-naphthoflavone inhibited the met The activity of microsomes pretreated with diphenytriazol for 4 d was similar to that in β-glucuronidase (P <0.05) naphthoflavone group, but was significantly different from those in control group and phenobarbital group. CONCLUSION: These results reveal that diphenytriazol is a novel inducer of CYP1A.