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Adult female standard dark mink were exposed to hexachlorobenzene (HCB) at concentrations of 0, 1, and 5 ppm in the feed and bred with males on the same treatments. Female offspring were allowed to mature to 16–17 weeks and killed. At 16–17 weeks of age, HCB had no effect on body weights or liver weights. Hepatic cytochrome P-450 and ethoxyresorufin-O-deethylase were significantly increased 2.0- and 1.5-fold, respectively, in the 5-ppm treatment group. Electron microscopy failed to reveal proliferation of the smooth endoplasmic reticulum. No hepatic damage was observed. No changes in in vitro renal function, measured as accumulation of para-aminohippurate and tetraethylammonium by renal cortical slices, were detected in any treatment group. Histological examination of renal slices did not reveal any alterations in morphology. Fat was the predominate site of HCB disposition; samples from the 5-ppm treatment group contained 626.10 ± 12.01 ng HCB/g tissue. Whereas perinatal HCB administration has profound effects on the survival of off-spring born to exposed mink, only induction of hepatic mixed-function oxidases was observed in the surviving kits without any observable frank hepatotoxicity.