ToxSci Advance Access originally published online on December 30, 2005
Toxicological Sciences 2006 90(2):490-499; doi:10.1093/toxsci/kfj085
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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
,

,1
* Marine & Freshwater Biomedical Sciences Center, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53204;
Great Lakes WATER Institute, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53204; and
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 female1 day1 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.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
T. C. King Heiden, J. Spitsbergen, W. Heideman, and R. E. Peterson Persistent Adverse Effects on Health and Reproduction Caused by Exposure of Zebrafish to 2,3,7,8-Tetrachlorodibenzo-p-dioxin During Early Development and Gonad Differentiation Toxicol. Sci., May 1, 2009; 109(1): 75 - 87. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Cohen, M. Shmoish, L. Levi, U. Cheruti, B. Levavi-Sivan, and E. Lubzens Alterations in Micro-Ribonucleic Acid Expression Profiles Reveal a Novel Pathway for Estrogen Regulation Endocrinology, April 1, 2008; 149(4): 1687 - 1696. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. J. McMillan and C. A. Bradfield The Aryl Hydrocarbon Receptor sans Xenobiotics: Endogenous Function in Genetic Model Systems Mol. Pharmacol., September 1, 2007; 72(3): 487 - 498. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Cheshenko, F. Brion, Y. Le Page, N. Hinfray, F. Pakdel, O. Kah, H. Segner, and R. I.L. Eggen Expression of Zebra Fish Aromatase cyp19a and cyp19b Genes in Response to the Ligands of Estrogen Receptor and Aryl Hydrocarbon Receptor Toxicol. Sci., April 1, 2007; 96(2): 255 - 267. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z. Shi, K. E. Valdez, A. Y. Ting, A. Franczak, S. L. Gum, and B. K. Petroff Ovarian Endocrine Disruption Underlies Premature Reproductive Senescence Following Environmentally Relevant Chronic Exposure to the Aryl Hydrocarbon Receptor Agonist 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Biol Reprod, February 1, 2007; 76(2): 198 - 202. [Abstract] [Full Text] [PDF] |
||||



