UBC Theses and Dissertations

UBC Theses Logo

UBC Theses and Dissertations

Effects on early in ovo 2,3,7,8-tetrachlorodibenzo-P-dioxin exposure on perinatal thyroid and sex steroid hormone levels in three avian species Janz, David Michael

Abstract

Halogenated aromatic hydrocarbons (HAHs) are a class of highly toxic and persistent environmental pollutants that include the polychlorinated dibenzo-p-dioxins (PCDDs), polychiorinated dibenzofiirans (PCDFs), and polychlorinated biphenyls (PCBs). Contamination of aquatic systems with these chemicals is believed to be responsible for impaired reproductive capacity in species at the top of the food web, such as fish-eating birds. A highly sensitive and specific biomarker of exposure to HAHs is the induction of cytochrome P4501A1 (CYP1A1) and associated hepatic microsomal ethoxyresorufin O-deethylase (EROD) activity. This thesis examined a number of toxicologically relevant hormonal endpoints, such as plasma thyroid and sex steroid hormone concentrations and hepatic estrogen receptor (ER) levels, as potential biomarkers of HAH exposure and toxic effect during the perinatal period in three avian species, in comparison to hepatic EROD induction. Since thyroid and sex steroid hormones are important in perinatal growth and development in avian species, perturbations in levels of these hormones during this period may be a factor in the decreased reproductive success observed in wild fish-eating bird species inhabiting aquatic systems contaminated with HAHs. Fertile eggs of the domestic chicken (Gallus gallus), pigeon (Columba livia), and great blue heron (Ardea herodias) were exposed early in incubation to the most toxic HAH, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Eggs were artificially incubated and sacrificed at relevant time points during the perinatal period. In chicken embryos and hatchlings exposed to 0.1 µg/kg of TCDD via air cell injection, hepatic EROD activity was induced half-maximally to maximally at all time points, indicating activation of the aryl hydrocarbon receptor (AhR) complex, an initial step in the mediation of TCDD toxicity. There were no effects of TCDD exposure on hatchability, plasma thyroid hormone (total T₃, total T₄), 17ß- estradiol, or testosterone concentrations, hepatic ER levels, or a number of body and skeletal growth-related parameters in chickens. In pigeons (1 µg/kg), hepatic EROD was induced half-maximally at hatch and day 7 after hatch. There were significant reductions in hatchability and several growth-related parameters in TCDD-exposed pigeons (p

Item Media

Item Citations and Data

Rights

For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.