ToxSci Advance Access originally published online on August 12, 2003
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Toxicological Sciences 76, 151-161 (2003)
Copyright © 2003 by the Society of Toxicology
REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY |
2,3,7,8-Tetrachlorodibenzo-p-dioxin Inhibits Zebrafish Caudal Fin Regeneration
,1
* School of Pharmacy, Department of Pharmaceutical Sciences, University of Colorado Health Sciences Center, Denver, Colorado 80262, and
Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon 97331
Adult zebrafish completely regenerate their caudal fins following partial amputation. Fin regrowth can easily be monitored in vivo and regenerating tissues can be used to study this dynamic developmental process. In this study we determined that fin regeneration is significantly affected by exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Zebrafish caudal fins were partially amputated, and the fish received intraperitoneal (ip) injection of 2.8, 14, or 70 ng/g weight TCDD or vehicle control. By 7 days postamputation, fish exposed to the highest concentration of TCDD regenerated 15% of their fin compared to 65% regrowth in control fish. To determine if this effect was stage specific, zebrafish were exposed to 70 ng/g TCDD on 1, 2, 3, or 4 days postamputation. Fin regeneration was significantly inhibited at all time points following TCDD exposure. TCDD exposure also induced hyperpigmentation in de novo tissue. Zebrafish were dosed with BrdU, following fin amputation and TCDD exposure, to study changes in cell proliferation. By 4 days postamputation, cell proliferation rates were significantly lower in TCDD-exposed fish. TCDD toxicity is mediated through the aryl hydrocarbon receptor (AHR), and RT-PCR experiments confirmed AHR2, ARNT2b, and TCDD-dependent CYP1A expression in the regenerating tissue. These results demonstrate that zebrafish caudal fin regeneration is a unique model to investigate molecular mechanism(s) of TCDD toxicity.
Key Words: zebrafish; fin regeneration; aryl hydrocarbon receptor; AHR; 2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  L. K. Mathew, S. Sengupta, A. Kawakami, E. A. Andreasen, C. V. Lohr, C. A. Loynes, S. A. Renshaw, R. T. Peterson, and R. L. Tanguay Unraveling Tissue Regeneration Pathways Using Chemical Genetics J. Biol. Chem., November 30, 2007; 282(48): 35202 - 35210. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. A. Andreasen, L. K. Mathew, C. V. Lohr, R. Hasson, and R. L. Tanguay Aryl Hydrocarbon Receptor Activation Impairs Extracellular Matrix Remodeling during Zebra Fish fin Regeneration Toxicol. Sci., January 1, 2007; 95(1): 215 - 226. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Villano and L. A. White The Aryl Hydrocarbon Receptor-Signaling Pathway and Tissue Remodeling: Insights from the Zebrafish (Danio rerio) Model System Toxicol. Sci., July 1, 2006; 92(1): 1 - 4. [Full Text] [PDF]
|
|
|
|
|
|
E. A. Andreasen, L. K. Mathew, and R. L. Tanguay Regenerative Growth Is Impacted by TCDD: Gene Expression Analysis Reveals Extracellular Matrix Modulation Toxicol. Sci., July 1, 2006; 92(1): 254 - 269. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. K. Mathew, E. A. Andreasen, and R. L. Tanguay Aryl Hydrocarbon Receptor Activation Inhibits Regenerative Growth Mol. Pharmacol., January 1, 2006; 69(1): 257 - 265. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|