PUBLICATION
Inhibition of Follicular Development, Vitellogenesis and Serum 17{beta} Estradiol Concentrations in Zebrafish Following Chronic, Sublethal Dietary Exposure to 2,3,7,8,-Tetrachlorodibenzo-p-dioxin
- Authors
- King Heiden, T., Carvan, M.J., 3rd, and Hutz, R.J.
- ID
- ZDB-PUB-060113-1
- Date
- 2006
- Source
- Toxicological sciences : an official journal of the Society of Toxicology 90(2): 490-499 (Journal)
- Registered Authors
- Carvan III, Michael J., King Heiden, Tisha
- Keywords
- TCDD, follicular development, estrogen and vitellogenin concentrations, zebrafish
- MeSH Terms
-
- Animals
- Body Burden
- Diet
- Endocrine Disruptors/pharmacokinetics
- Endocrine Disruptors/toxicity
- Environmental Pollutants/pharmacokinetics
- Environmental Pollutants/toxicity*
- Estradiol/blood*
- Female
- Fertility/drug effects
- Liver/drug effects
- Liver/pathology
- Male
- Ovarian Follicle/drug effects*
- Ovarian Follicle/growth & development
- Vitellogenins/blood*
- Zebrafish
- PubMed
- 16387744 Full text @ Toxicol. Sci.
Citation
King Heiden, T., Carvan, M.J., 3rd, and Hutz, R.J. (2006) Inhibition of Follicular Development, Vitellogenesis and Serum 17{beta} Estradiol Concentrations in Zebrafish Following Chronic, Sublethal Dietary Exposure to 2,3,7,8,-Tetrachlorodibenzo-p-dioxin. Toxicological sciences : an official journal of the Society of Toxicology. 90(2):490-499.
Abstract
The environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent endocrine disruptor with the ability to disrupt several biologic processes, including reproduction. In fish, sublethal exposure to TCDD is known to modulate overall reproductive capacity, but impacts on follicular development and vitellogenesis are unknown. Here we show that chronic, dietary exposure to 0.08, 0.32, or 0.80 ng TCDD female(-1) day(-1) decreased egg production by more than 50% and that spawning success was reduced by as much as 96%. Serum estradiol concentrations were decreased by more than 2-fold accounting for, in part, observed decreases in serum vitellogenin concentrations by as much as 29%. Our data suggest that decreased egg production is likely the result of TCDD-mediated inhibition of the transition from pre-vitellogenic stage to vitellogenic stage follicles, as well as the induction of follicular atresia. While the majority of reproductive toxicity of TCDD is likely due to direct impacts on the ovary, histopathologic observations suggest liver toxicity could also contribute to observed impacts on vitellogenesis. Importantly, even when overall egg production is not significantly impacted, our data show that subtle physiologic changes induced by TCDD can lead to altered gonadogenesis, suggesting that long-term exposure to very low concentrations of TCDD could greatly impact fecundity and reproductive success in fishes.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping