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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

University of British Columbia

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<0.01), but no effect on plasma thyroid hormone, estradiol, or testosterone concentrations, or hepatic ER levels. In great blue herons (2 µg/kg) sacrificed at hatch and day 7, hepatic EROD activity was elevated three- and two-fold above controls, respectively, similar to EROD induction observed in heron hatchlings exposed to environmental levels of HAHs in the Strait of Georgia, BC. In TCDD-exposed herons, there were elevated hepatic ER concentrations (Bmax) and decreased ER affinities (Kd) at hatch (p<0.05), but not on day 7 after hatch. Liver[³H]-TCDD concentrations decreased 14-fold between hatch and day 7. There was no effect of TCDD exposure on plasma thyroid hormone, estradiol, or testosterone concentrations in herons. In a separate experiment, pigeons were exposed during the latter third part of incubation to a TCDD dose (3 µg/kg) which would cause high embryo mortality if exposure occurred early in incubation. In this experiment, hepatic EROD was induced half-maximally at hatch and day 7. Plasma total T₃ and estradiol levels were decreased at hatch, and estradiol was elevated on day 7 in TCDD-exposed pigeons (p<0.05). Similar to herons, hepatic ER concentrations were increased at hatch (p<0. 01). Overall, the results of this thesis consistently show that in chickens, pigeons, and great blue herons exposed to TCDD early in incubation, thyroid and sex steroid hormone concentrations are not as sensitive as hepatic EROD activity, body growth, or mortality as biomarkers of exposure. However, the results suggest that TCDD may influence hepatic ER levels during the perinatal period in certain avian species.

Thesis/Dissertation

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2009-04-16

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http://hdl.handle.net/2429/7242

Pharmaceutical Sciences

University of British Columbia

UBCV

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