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ToxSci Advance Access originally published online on December 30, 2005
Toxicological Sciences 2006 90(2):490-499; doi:10.1093/toxsci/kfj085
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Inhibition of Follicular Development, Vitellogenesis, and Serum 17ß-Estradiol Concentrations in Zebrafish Following Chronic, Sublethal Dietary Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin

Tisha King Heiden*,{dagger},{ddagger}, Michael J. Carvan, III*,{dagger} and Reinhold J. Hutz{ddagger},1

* Marine & Freshwater Biomedical Sciences Center, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53204; {dagger} Great Lakes WATER Institute, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53204; and {ddagger} Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53211

Received October 10, 2005; accepted December 20, 2005

The environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent endocrine disruptor with the ability to affect 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 more than twofold, accounting, in part, for 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 follicles to vitellogenic stage follicles, as well as the induction of follicular atresia. The majority of reproductive toxicity of TCDD is likely due to direct impacts on the ovary, yet histopathologic observations suggest liver toxicity could also contribute to observed impacts on vitellogenesis. Importantly, even when overall egg production is not significantly affected, our data show that subtle physiologic changes induced by TCDD can lead to altered gonadogenesis. This suggests that long-term exposure to very low concentrations of TCDD could greatly affect fecundity and reproductive success in fishes.

Key Words: TCDD; follicular development; estrogen and vitellogenin concentrations; zebrafish.


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