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Biochemical markers for differentiation of exposures to nonplanar polychlorinated biphenyls, organochlorine pesticides, or 2,3,7, 8-tetrachlorodibenzo-p-dioxin in trout liver.

The effects of a single intraperitoneal dose of the prototypical contaminant nonplanar 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153, 50 mg/kg), p,p'-DDE (50 mg/kg), or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 200 ng/kg) on the activities of hepatic detoxification enzymes were examined in the liver of immature rainbow trout (Oncorhynchus mykiss). Different modulations of the tested xenobiotics on microsomal cytochrome P450-dependent testosterone hydroxylase activities were found: PCB 153 specifically induced 16beta-hydroxylase activity, whereas p,p'-DDE decreased cytochrome P4503A-dependent 6beta-hydroxylation as well as 16alpha- and 2alpha-hydroxylation. TCDD did not modulate testosterone hydroxylase activities, but a strong induction of cytochrome P4501A activity was observed after TCDD administration; hence, cytochrome P4501A is not involved in the hydroxylation of testosterone. Trout hepatic microsomal glutathione S-transferase (GST) activity, enhanced by all the xenobiotics tested, was found to be a sensitive nonspecific biochemical marker of oxidative stress; cytosolic glutathione reductase was a less sensitive indicator of oxidative stress and was induced significantly only by treatment with p,p'-DDE. Cytosolic GST activity toward ethacrynic acid (GST-ETHA) was induced by PCB 153 or p,p'-DDE, but not by TCDD. Modulations of hepatic microsomal testosterone hydroxylase activities and induction of GST-ETHA appeared to be suitable biochemical markers of acute exposure to nonplanar PCBs and organochlorines that do not induce cytochrome P4501A enzymes in rainbow trout, whereas microsomal GST and cytosolic glutathione reductase may become early biochemical indicators of oxidative stress.