EFFECTS OF EMBRYONIC AND ADULT EXPOSURE TO 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN ON HEPATIC-MICROSOMAL TESTOSTERONE HYDROXYLASE-ACTIVITIES INGREAT BLUE HERONS (ARDEA-HERODIAS)

In a continuing effort to evaluate biomarkers of exposure of great blu e herons (Ardea herodias) to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD ) and related halogenated aromatic hydrocarbons, we examined the effec t of TCDD on hepatic microsomal testosterone hydroxylase activities. H eron embryos were exposed in ovo to 2 mu g TCDD/kg egg (or corn oil ve hicle) and sacrificed at hatch or 7 d posthatch. Adult herons were exp osed intraperitoneally to 20 mu g TCDD/kg and sacrificed 2 weeks later . The sex of the birds was known for the adults only. Hepatic microsom es of herons of each age group were able to hydroxylate testosterone a t the 2 beta, 6 beta, 15 alpha, 16 alpha, or 16 beta positions. In 7-d -old chicks, an additional unidentified compound was formed. The age o f the untreated herons had a strong influence on the activities of the five hydroxylases with changes of up to 17-fold. The TCDD significant ly (p < 0.05) induced 2 beta-, 6 beta-, and 15 alpha-testosterone hydr oxylase activities in the adult females, 15 alpha- in the adult males, and 6 beta-testosterone hydroxylase activity in the hatchlings. In th e 7-d-old chicks. induction was no longer apparent. A significant corr elation existed between hepatic microsomal ethoxyresorufin O-deethylas e (EROD) and 6 beta-testosterone hydroxylase activity in hatchlings (r = 0.91; n = 12) and adult female herons (r = 1.0; n = 4). The TCDD-in duced changes in testosterone hydroxylase activities occurred at doses that resulted in tissue concentrations and levels of EROD induction t hat were environmentally relevant, but did not result in overt toxicit ies.