Dietary 2,3,7,8-tetrachlorodibenzofuran in rainbow trout: accumulation, disposition, and hepatic mixed-function oxidase enzyme induction.

Juvenile rainbow trout (Oncorhynchus mykiss) were exposed to dietary 2,3,7,8-[3H]tetrachlorodibenzofuran (TCDF) (0.36 to 42.8 ng g-1) and accumulation, tissue distribution, biotransformation, and hepatic monooxygenase enzyme (MO) induction were studied. The assimilation efficiency of TCDF ranged from 49 to 62% in 30-day exposures and was independent of the TCDF level in the diet. Depuration half-lives (whole body) of TCDF following 30-day exposure ranged from 40 to 77 days and were significantly more rapid in fish exposed to 42.8 ng g-1. Liver somatic index (LSI) and rate of increase in liver weight were elevated in fish exposed to 42.8 ng g-1 TCDF compared to controls. Exposure to 9.2 ng g-1 TCDF in the diet for 140 days also resulted in higher LSI values, as well as increased mortality (16%), but had no significant effects on growth. [3H]TCDF was found mainly in the carcass (63-74%) and GI tract (18-31%), with lesser amounts in liver (0.6-2.3%) during the 140-day exposure, primarily (> 98%) in the form of the parent compound. Radioactivity in bile was found mainly as a single polar transformation product by reverse-phase HPLC. Glucuronidase hydrolysis yielded a product with the retention time expected of hydroxylated TCDF, suggesting the presence of a glucuronide conjugate. MO enzyme induction measured by ethoxyresorufin-O-deethylase (EROD) activity in liver (postmitochondrial supernatant) was 137.5 and 15 times higher than that in control fish after 30 days dietary exposure to 42.8 and 9.2 ng g-1, respectively. EROD activities were correlated with TCDF concentrations in liver (R2 = 0.59, N = 45).