HEPATIC-MICROSOMAL ETHOXYRESORUFIN O-DEETHYLASE-INDUCING POTENCY IN OVO AND CYTOSOLIC AH RECEPTOR-BINDING AFFINITY OF 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN - COMPARISON OF 4 AVIAN SPECIES

The hepatic microsomal ethoxyresorufin O-deethylase (EROD)-inducing po tency in ovo of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was determi ned in the domestic chicken (Gallas gallus), domestic pigeon (Columba livia), great blue heron, and double-crested cormorant. Dose-response curves were produced by injecting various doses of [H-3]TCDD into the air sac of developing eggs during the latter third part of incubation. Hepatic EROD activities were measured in day-old hatchlings. Liver, y olk, and whole blood were analyzed for [H-3]TCDD; no distributional di fferences among species were found. The ED50 for EROD induction was be tween one and two orders of magnitude lower in the chick (0.1 mu g/kg egg) than in the heron and cormorant (3-10 mu g/kg egg). Consistent wi th this, the apparent affinity of TCDD for the hepatic cytosolic Ah re ceptor was about 15 times higher in the domestic chick (K-d = 0.75-1.6 ) than in the other avian species (pigeon, K-d = 11-14; heron, K-d = 1 020; cormorant, K-d = 12-16). Receptor binding affinities in the pigeo n, heron, and cormorant were of the same order of magnitude as that re ported for human placenta (D. K. Manchester, S. K. Gordon, C. L. Golas , E. A. Roberts, and A. B. Okey, 1987, Cancer Res. 47, 4861-4868). Sub cutaneous edema was observed in TCDD-treated hatchlings of the chick, heron, and cormorant, but not of the pigeon, within the dose range exa mined. The laboratory dose-response relationships demonstrated that th e heron and cormorant hatchlings that were exposed to TCDD and related chemicals in the Strait of Georgia (J. T. Sanderson, R. J. Norstrom, J. E. Elliott, L. E. Hart, K. M. Cheng, and G. D. Bellward (1994b) J. Toxicol. Environ. Health 41, 245-263; and J. T. Sanderson, J. E. Ellio tt, R. J. Norstrom, P. E. Whitehead, L. E. Hart, K. M. Cheng, and G. D . Bellward (1994a) J. Toxicol. Environ. Health 41, 435-450) had hepati c EROD activities at the lower end of the linear part of their respect ive dose-response curves. A further increase in levels of TCDD and re lated compounds in the environment would lead to a large increase in E ROD activity and further increases in TCDD-induced toxicities, such as body weight loss and subcutaneous edema. (C) 1995 Academic Press, Inc .