Toxicol Appl Pharmacol. 1996 Aug;139(2):292-300.
In Ovo 2,3,7,8-Tetrachlorodibenzo-p-dioxin Exposure in Three Avian Species.
Toxicology and applied pharmacology
- Division of Pharmacology and Toxicology, University of British Columbia, Vancouver, British Columbia, V6T 1Z3, Canada
As opposed to mammals, the heterogametic sex in birds is female, and sexual differentiation of the central nervous system away from the intrinsic male pattern is dependent on ovarian estrogen secretions during the perinatal period. The contamination of aquatic systems with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds has been suggested to be responsible for decreased reproductive success in certain wild fish-eating bird populations. Since TCDD has been shown to alter estrogenic status in laboratory animals, we determined the effects of in ovo TCDD exposure on hepatic estrogen receptor (ER) concentrations and affinities, and plasma estradiol concentrations during the perinatal period in the domestic chicken (Gallus gallus), domestic pigeon (Columba livia), and great blue heron (Ardea herodias). Plasma testosterone levels were also determined in herons as an indication of androgenic status. [3H]TCDD was injected into the air cell of chicken eggs on Embryonic Day 4.5 (0.1 μg/kg egg), pigeon eggs on Embryonic Day 3.5 (1 μg/kg egg) and Embryonic Day 14 (3 μg/kg egg), and heron eggs at approximately Embryonic Day 13 (2 μg/kg egg). Chickens were euthanized on Embryonic Days 17 and 19, hatch, and Days 2 and 4 after hatch. Pigeons and herons were either euthanized at hatch or fed an uncontaminated diet for 7 days prior to termination. Between 5 and 10% of the injected [3H]TCDD dose was measured in the liver of hatchlings. There was no effect of in ovo TCDD exposure on hepatic ER levels or plasma estradiol concentrations in female chickens and pigeons exposed early in incubation. In female pigeons exposed during the latter third part of incubation to a TCDD dose that would cause high embryo lethality if injected early in incubation, hepatic ER concentrations were elevated (p < 0.001) and plasma estradiol concentrations were decreased (p < 0.01) at hatch. There was no effect of TCDD exposure on plasma estradiol levels in male pigeons. In herons, TCDD exposure had no effect on hepatic ER levels or plasma estradiol and testosterone concentrations at either time point. We conclude that in chicken, pigeon, and great blue heron hatchlings exposed early in incubation to low doses of TCDD, hepatic ER levels and plasma estradiol concentrations are not biomarkers of toxicity.