We examined the effects of handling induced-stress combined with tetrachlorobiphenyl (TCB) exposure and the effects of long-term exposure to PCB on selected detoxification enzymes in the liver and kidney, and on the head kidney 21-hydroxylation of a 17-alpha-hydroxyprogesterone, an enzymatic step in cortisol biosynthesis in rainbow trout (Oncorhynchus mykiss). Our findings suggest that experimental conditions, such as stress, play an important role in mediating detoxification responses in rainbow trout. TCB together with stress caused significantly elevated liver etoxyresorufin-O-deethylase (EROD) and etoxycoumarine-O-deethylase (ECOD) activities, whereas 14 days TCB treatment alone did not alter the enzyme activities significantly. The UDP-glucuronosyltransferase (UGT) activity increased significantly in fish recovering from stress. The 21-hydroxylation of a 17-alpha-hydroxyprogesterone was not affected by TCB, stress or by PCB. The induced ECOD activity could be inhibited by alpha NF to control levels, indicating the existence of a non-inducible form of CYP exhibiting ECOD activity. Long-term exposure to PCBs induced UGT, glutathione reductase (GR) and glutathione tansferase (GT) activities in the liver. The rapid induction of UGT by TCB compared with PCB suggests that TCB is a potent UGT-inducing congener in the PCB mixture. The different induction patterns of CYP-dependent activities and the GR, GT and UGT activities suggest differential regulation of these enzymatic activities. (C) 1997 Elsevier Science B.V.