Abstract

Juvenile rainbow trout ( Oncorhynchus mykiss) and lake whitefish ( Coregonus clupeaformis) were exposed to three concentrations (40, 190, 400 pg g −1) of dietary 2,3,7,8-[ 3 H] tetrachlorodibenzo-p-dioxin (TCDD) to compare bioaccumulation and hepatic monooxygenase enzyme (MO) induction. Fish were exposed for 30 days followed by a 180 day depuration phase. Differences in the accumulation and depuration of TCDD were found between rainbow trout and lake whitefish, despite similar body size and lipid content. Assimilation efficiencies of TCDD were greater in lake whitefish (66–76%) than rainbow trout (43–58%), but TCDD half lives were shorter in lake whitefish (32–39 days) than in rainbow trout (73–83 days). Biomagnification factors (BMF) ranged from 1.6 to 1.8 in rainbow trout and from 0.8 to 0.9 in lake whitefish, confirming the known potential for biomagnification of TCDD in aquatic food webs. Reverse phase HPLC showed that a majority of the radioactivity in the rainbow trout bile was TCDD, with minor amounts present as a hydroxylated TCDD and as a glucuronide conjugate. MO enzyme induction, measured by ethoxyresorufin- O-deethylase (EROD), was observed in the rainbow trout after 10 days of exposure to 400 pg g −1 TCDD, and in the lake whitefish after 5 days of exposure to 380 pg g −1 TCDD. The whole fish threshold concentration for EROD induction by TCDD ranged between 15 and 45 pg g −1 (wet weight) for both species. EROD activity returned to control levels 120 and 80 days after the cessation of the treatments in the rainbow trout and lake whitefish, respectively. Growth rates were significantly reduced in trout and whitefish at whole fish concentrations (wet weight) of 150 ± 4.6 and 85 ± 8.3 pg g −1, respectively. Histological effects of the TCDD were found in the spleen and liver of the rainbow trout which had whole fish concentrations (wet weight) of 150 ± 4.6 pg mg −1and 72 ± 8.0 pg mg −1 TCDD, respectively.

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