title: In ovo 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure in three avian species. 1. Effects on thyroid hormones and growth during the perinatal period.
abstract: Thyroid hormones are important in the perinatal growth and development of avian species, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds have been shown to cause alterations in these hormones in laboratory animals. Since the decreased reproductive success in certain fish-eating bird populations exposed to TCDD and related compounds is characterized by high embryo and hatchling mortality, we examined the effects of in ovo TCDD exposure on plasma thyroid hormone concentrations (total T3, total T4) and body and skeletal growth during the perinatal period in the domestic chicken (Gallus gallus), domestic pigeon (Columba livia), and great blue heron (Ardea herodias). Hepatic ethoxyresorufin O-deethylase (EROD) activity was also determined as an enzymatic marker of cytochrome P450IA induction by TCDD. [3H]TCDD was injected into the air cell of chicken eggs (21-day incubation period) on Embryonic Day 4.5 (0.1 microgram/kg egg), pigeon eggs (18-day incubation period) on Embryonic Day 3.5 (1 microgram/kg egg) and Embryonic Day 14 (3 microgram/kg egg), and heron eggs (28-day incubation period) at approximately the midpoint of incubation (2 microgram/kg egg). Chickens were euthanized on Embryonic Days 17 and 19, day of hatch (Embryonic Day 21), and Days 2 and 4 after hatch. Pigeons and herons were euthanized either at hatch (Embryonic Days 18 and 28, respectively), or fed an uncontaminated diet for 7 days prior to sacrifice. Although hepatic EROD activity was induced 13- to 43-fold above controls in chickens, there was no effect of TCDD exposure on hatchability, body growth, subcutaneous edema, or plasma thyroid hormone levels. In pigeons exposed to TCDD on Embryonic Day 3.5, EROD was induced 6- to 15-fold, hatchability was decreased, liver to body weight ratio was elevated, and body and skeletal growth were decreased (p < 0.01); however, there was no effect of TCDD exposure on plasma thyroid hormone levels. Similarly, in pigeons exposed to TCDD on Embryonic Day 14, EROD was induced 10- to 14-fold, liver to body weight ratio was elevated, and body and skeletal growth were decreased (p < 0.01), but there was no effect of TCDD treatment on plasma thyroid hormone levels. In herons, hepatic EROD activity was induced 2- to 3-fold above control birds, similar to EROD activities measured in heron hatchlings exposed to environmental levels of TCDD and related chemicals in the Strait of Georgia, British Columbia. However, this level of TCDD exposure had no effect on plasma thyroid hormone levels or body growth in herons. Collectively, these results suggest that perinatal plasma thyroid hormone levels cannot be used as relatively noninvasive biomarkers of TCDD exposure during embryonic development in chickens, pigeons, and great blue herons.
authors.affiliation: Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.
authors.forename: D M
authors.initials: DM
authors.lastname: Janz
authors.forename: G D
authors.initials: GD
authors.lastname: Bellward
mesh_terms: D000014:Abnormalities, Drug-Induced; D000818:Animals; D001717:Birds / Q000002:abnormalities* / Q000196:embryology; D002642:Chick Embryo; D010856:Columbidae; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D004487:Edema / Q000139:chemically induced; D004625:Embryo, Nonmammalian / Q000187:drug effects* / Q000196:embryology; D047108:Embryonic Development; D005298:Fertility / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D010063:Ovum / Q000187:drug effects* / Q000502:physiology; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D013961:Thyroid Gland / Q000187:drug effects* / Q000503:physiopathology; D013963:Thyroid Hormones / Q000097:blood / Q000502:physiology*
chemical_list: D000072317:Polychlorinated Dibenzodioxins; D013963:Thyroid Hormones; D019363:Cytochrome P-450 CYP1A1