Skip Navigation



ToxSci Advance Access published online on January 12, 2004

Toxicological Sciences, doi:10.1093/toxsci/kfh056
Toxicological Sciences © Society of Toxicology 2004; all rights reserved
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
78/1/78    most recent
kfh056v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Hill, A. J.
Right arrow Articles by Heideman, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hill, A. J.
Right arrow Articles by Heideman, W.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received October 9, 2003; accepted December 4, 2003
© 2004 Society of Toxicology

Environmental Toxicology

Water Permeability and TCDD-Induced Edema in Zebrafish Early Life Stages

Adrian J. Hill 1, Susan M. Bello 1, Amy L. Prasch 2, Richard E. Peterson 1, and Warren Heideman 1*

1 School of Pharmacy, University of Wisconsin, Madison, Wisconsin 53705
2 Molecular and Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin 53705

* To whom correspondence should be addressed. E-mail: wheidema{at}wisc.edu.


   Abstract

A common response to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in teleost embryos is blue sac disease, characterized by pericardial and yolk sac edema. The cellular and extracellular fluids of freshwater fish are hyperosmotic compared to the surrounding water. In order to maintain an osmotic balance, freshwater fish must maintain a barrier to minimize water entry and excrete excess water that passes the barrier. We hypothesized that edema observed in TCDD-exposed zebrafish was caused by a failure of a barrier to incoming water. As a test of this hypothesis, we removed the osmotic gradient that drives water entry by increasing the osmolarity of the surrounding water with mannitol. Abolishing the osmotic gradient between the interior body fluids and the water environment of the developing zebrafish significantly reduced both pericardial and yolk sac edema. When added after edema formation had already started, mannitol only partially reversed preexisting edema. An alternate hypothesis is that TCDD impairs water excretion, allowing water to accumulate as edema fluid. However, we were unable to demonstrate an alteration in kidney function: expression of early markers for kidney development appeared normal, and we did not observe TCDD-induced changes in kidney filtration. An alteration in the overall shape of the kidney was observed, but this may be a consequence of compression by edema. In conclusion, TCDD exposure may inhibit the function of a permeability barrier to water that is critical for maintaining osmotic balance in early development

Key Words: AHR2, ARNT2, TCDD, zebrafish, blue sac syndrome, edema .


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Toxicol SciHome page
A. C. Grimes, K. N. Erwin, H. A. Stadt, G. L. Hunter, H. A. Gefroh, H.-J. Tsai, and M. L. Kirby
PCB126 Exposure Disrupts ZebraFish Ventricular and Branchial but Not Early Neural Crest Development
Toxicol. Sci., November 1, 2008; 106(1): 193 - 205.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
S. M. Billiard, J. N. Meyer, D. M. Wassenberg, P. V. Hodson, and R. T. Di Giulio
Nonadditive effects of PAHs on Early Vertebrate Development: mechanisms and implications for risk assessment
Toxicol. Sci., September 1, 2008; 105(1): 5 - 23.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
T. K. Heiden, R. J. Hutz, and M. J. Carvan III
Accumulation, Tissue Distribution, and Maternal Transfer of Dietary 2,3,7,8,-Tetrachlorodibenzo-p-Dioxin: Impacts on Reproductive Success of Zebrafish
Toxicol. Sci., October 1, 2005; 87(2): 497 - 507.
[Abstract] [Full Text] [PDF]


Home page
DevelopmentHome page
A. Holtzinger and T. Evans
Gata4 regulates the formation of multiple organs
Development, September 1, 2005; 132(17): 4005 - 4014.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
A. J. Hill, H. Teraoka, W. Heideman, and R. E. Peterson
Zebrafish as a Model Vertebrate for Investigating Chemical Toxicity
Toxicol. Sci., July 1, 2005; 86(1): 6 - 19.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
D. S. Antkiewicz, C. G. Burns, S. A. Carney, R. E. Peterson, and W. Heideman
Heart Malformation Is an Early Response to TCDD in Embryonic Zebrafish
Toxicol. Sci., April 1, 2005; 84(2): 368 - 377.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
A. L. Prasch, W. Heideman, and R. E. Peterson
ARNT2 Is Not Required for TCDD Developmental Toxicity in Zebrafish
Toxicol. Sci., November 1, 2004; 82(1): 250 - 258.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.