2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) was administered intragastrically twice with 4 days interval, to juvenile cod and rainbow trout, total dose 8 mug/kg body weight. Fish were killed after 9 and 17 days and the effects on hepatic xenobiotic metabolizing enzymes were determined by examining aldrin epoxidase (AE), glutathione-S-transferase (GST) against 1-chloro-2,4-dinitrobenzene (CDNB) and the cytochrome P450-dependent ethoxyresorufin-O-deethylase (EROD) activities, and by immunoquantitating cytochrome P4501A1 using an indirect enzyme-linked immunosorbent assay (ELISA). AE and GST activities were not induced. However, 2,3,7,8-TCDD significantly induced EROD activities in rainbow trout and cod to 1450% and 415%, respectively, of the corresponding controls 9 days after the first treatment. The increase in EROD activity was supported by induction of the main catalyst P4501A1 as revealed by ELISA analyses. The distribution pattern of C-14-labelled 2,3,7,8-TCDD was studied by whole-body autoradiography. The liver concentration of radiolabelled compound in cod exceeded that of the rainbow trout. However, the degree of hepatic enzyme induction did not correspond to the concentration of radiolabelled 2,3,7,8-TCDD in the liver. Despite of the substantially higher level of 2,3,7,8-TCDD in the liver of cod, the EROD induction was lower in this species compared to rainbow trout.