Effects of embryonic and adult exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin on hepatic microsomal testosterone hydroxylase activities in great blue herons (Ardea herodias)

Abstract

AbstractIn a continuing effort to evaluate biomarkers of exposure of great blue herons (Ardea herodias) to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) and related halogenated aromatic hydrocarbons, we examined the effect of TCDD on hepatic microsomal testosterone hydroxylase activities. Heron embryos were exposed in ovo to 2 μg TCDD/kg egg (or corn oil vehicle) and sacrificed at hatch or 7 d posthatch. Adult herons were exposed intraperitoneally to 20 μg TCDD/kg and sacrificed 2 weeks later. The sex of the birds was known for the adults only. Hepatic microsomes of herons of each age group were able to hydroxylate testosterone at the 2β, 6β, 15α, 16α, or 16β positions. In 7‐d‐old chicks, an additional unidentified compound was formed. The age of the untreated herons had a strong influence on the activities of the five hydroxylases, with changes of up to 17‐fold. The TCDD significantly (p < 0.05) induced 2β‐, 6β‐, and 15α‐testosterone hydroxylase activities in the adult females, 15α‐ in the adult males, and 6β‐testosterone hydroxylase activity in the hatchlings. In the 7‐d‐old chicks, induction was no longer apparent. A significant correlation existed between hepatic microsomal ethoxyresorufin O‐deethylase (EROD) and 6β‐testosterone hydroxylase activity in hatchlings (r = 0.91; n = 12) and adult female herons (r = 1.0; n = 4). The TCDD‐induced changes in testosterone hydroxylase activities occurred at doses that resulted in tissue concentrations and levels of EROD induction that were environmentally relevant, but did not result in overt toxicities.