- Library Home /
- Search Collections /
- Open Collections /
- Browse Collections /
- UBC Theses and Dissertations /
- Effects on early in ovo 2,3,7,8-tetrachlorodibenzo-P-dioxin...
Open Collections
UBC Theses and Dissertations
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 Metadata
Title |
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
|
Creator | |
Publisher |
University of British Columbia
|
Date Issued |
1994
|
Description |
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
|
Extent |
2809598 bytes
|
Genre | |
Type | |
File Format |
application/pdf
|
Language |
eng
|
Date Available |
2009-04-16
|
Provider |
Vancouver : University of British Columbia Library
|
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.
|
DOI |
10.14288/1.0088045
|
URI | |
Degree (Theses) | |
Program (Theses) | |
Affiliation | |
Degree Grantor |
University of British Columbia
|
Graduation Date |
1995-11
|
Campus | |
Scholarly Level |
Graduate
|
Aggregated Source Repository |
DSpace
|
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.