Toxicological manifestations of 2,4,5,‐2’,4’,5'‐, 2,3,6,2’,3’,6'‐, and 3,4,5,3’,4’,5'‐hexachlorobiphenyl and Aroclor 1254 in mink

Abstract

Adult female mink were fed diets that contained 2.5 ppm Aroclor 1254, 0.1 or 0.5 ppm 3,4,5,3’,4’,5'‐hexachlorobiphenyl (345 HCB), 2.5 or 5.0 ppm 2,4,5,2’,4’,5'‐hexa‐chlorobiphenyl (245 HCB) or 2,3,6,2’,3’,6'‐hexachlorobiphenyl (236 HCB), or a control diet from 1 mo prior to breeding through parturition. All mink fed 0.5 ppm 345 HCB died within 60 d, while those fed 0.1 ppm showed 50% mortality after 3 mo exposure. Only one stillborn kit was whelped in the Aroclor 1254 group. No adverse reproductive effects were observed in the animals fed 236 HCB or 245 HCB. Plasma progesterone concentrations were significantly depressed by Aroclor 1254 and significantly elevated by 0.1 ppm 345 HCB. 170‐Estradiol concentrations were not significantly altered by any of the dietary treatments. Hepatic microsomal cytochrome P‐450 concentrations were significantly elevated by all treatments except 236 HCB, with the largest increases occurring in mink exposed to Aroclor 1254 and 345 HCB. Aminopyrine N‐demethylase activity was elevated by 5.0 ppm 245 HCB. Aroclor 1254 caused significant elevations in both benzo[a]pyrene hydroxyiase and ethoxyresorufin O‐deethylase activities. Benzo[a]pyrene hydroxyiase activities were also significantly elevated in mink fed 245 HCB and 345 HCB. Aroclor 1254 caused a significant elevation in cerebellar and hypothalamic norepinephrine concentrations and a significant elevation in hypothalamic dopamine concentrations. Cerebral dopamine was elevated by 0.1 ppm 345 HCB, while midbrain dopamine levels were depressed. Norepinephrine concentrations were significantly elevated by 5.0 ppm 236 HCB in the midbrain and by 5.0 ppm 245 HCB in the medulla.