Accumulation, tissue distribution, and depuration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-derived 3H were examined in fingerling yellow perch fed a diet containing 494 ppt of [3H]TCDD for 13 weeks followed by the same diet without TCDD for 13 weeks. None of the TCDD-exposed perch showed any signs of overt toxicity such as reduced growth rate, fin necrosis, cutaneous hemorrhage, or lethality. At the end of the 13-week exposure period, 78% of the total body burden of TCDD-derived 3H was contained in the carcass and visceral fat while the remaining 22% was distributed among the liver (9%), gill (5%), skin (3%), skeletal muscle (2%), gastrointestinal tract (1%), pyloric caeca (1%), kidney (less than 1%), spleen (less than 1%), and heart (less than 1%). High-performance liquid chromatographic analysis of organic extracts of visceral fat, carcass, liver, skeletal muscle, and skin showed that 96-99% of the tritium extracted from these tissues was due to the parent compound. The estimated t1/2 for whole-body depuration of TCDD-derived 3H was 18 weeks, and individual organ t1/2 values ranged from 6 to 19 weeks for the gastrointestinal tract, pyloric caeca, liver, gill, and carcass, and from 24 to 49 weeks for the visceral fat, kidney, skin, skeletal muscle, and spleen. To determine if yellow perch metabolize TCDD, a single dose of [14C]TCDD was administered to adult yellow perch (60 micrograms/kg, ip), and, 1 week later, gallbladder bile, liver, skeletal muscle, and kidney were removed, extracted, and analyzed by high-performance liquid chromatography. In contrast to the liver, muscle, and kidney where the parent compound accounted for 96-99% of the extractable 14C, the gallbladder bile contained almost entirely TCDD metabolites. At least four TCDD metabolites were detected in yellow perch bile and beta-glucuronidase treatment of the bile suggested that at least one was a glucuronide conjugate.