Abstract
1. In vivo treatment of chicks, quail and rats with 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) or 3-methylcholanthrene (MC) caused a dose-dependent increase in hepatic microsomal aryl hydrocarbon hydroxylase activity. 2. A much lower level of AHH induction was observed following similar treatment of trout with high concentrations of TCDD or MC. 3. No induction was apparent in midgut tissues from southern armyworm larvae exposed to the same inducers. 4. A low level of receptor exhibiting specific binding of [ 3H]TCDD was demonstrated in chick hepatic cytosol, but no evidence of receptor was obtained with the other species. 5. Although the specific binding of the receptor in chick eytosol was only 6–8 fmoles TCDD bound/mg protein compared to 135 fmoles/mg in rat hepatic cytosol, the chick receptor exhibited properties similar to those of Ah receptors in mammals.
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