Metabolism and disposition of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rainbow trout

Accumulation, tissue distribution, and depuration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-derived ³H were studied in fingerling rainbow trout fed a diet containing 494 ppt [³H]TCDD for 13 weeks followed by the same diet without TCDD for 13 weeks. This exposure did not cause fin rot, cutaneous hemorrhage, reduced growth rate, or an increase in relative lethality in TCDD-exposed fish. Visceral fat, carcass, skin, and pyloric caeca and all fatty tissues, accounted for greater than 90% of the TCDD-derived ³H in the fish after the 13 week exposure period. The remaining TCDD-derived radioactivity was distributed to skeletal muscle, gill, gastrointestinal tract, liver, kidney, heart, and spleen. High-pressure liquid chromatographic analysis of ³H in skeletal muscle, liver, kidney, carcass, and visceral fat showed that it was primarily due to TCDD (≥98%) and not metabolites (≤2%). The t 1 2 for whole-body depuration of TCDD-derived ³H was 15 weeks, and individual organ t 1 2 values ranged from 8 to 19 weeks. To determine if rainbow trout metabolize TCDD, adult fish were injected with [¹⁴C]TCDD (60 μg/kg, ip), and gallbladder bile, liver, skeletal muscle, and kidney were analyzed 1 week later. While only the parent compound was found in the tissues, bile contained at least three TCDD metabolites and the parent compound. β-Glucuronidase treatment of the bile suggested that at least one TCDD metabolite was a glucuronide conjugate.