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ToxSci Advance Access published online on August 12, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg205
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received June 11, 2003; accepted July 18, 2003
© 2003 Society of Toxicology

Reproductive and Developmental Toxicology

2,3,7,8-Tetrachlorodibenzo-p-dioxin Inhibits Zebrafish Caudal Fin Regeneration

Jeanmarie M. Zodrow 1 and Robert L. Tanguay 2*

1 School of Pharmacy, Department of Pharmaceutical Sciences, University of Colorado Health Sciences Center, Denver, CO 80262
2 Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331

* To whom correspondence should be addressed. E-mail: robert.tanguay{at}oregonstate.edu.


  Abstract

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 were intraperitoneal (i.p.) injection with 2.8, 14 or 70 ng/g weight TCDD or vehicle control. By 7 days post amputation, 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 post amputation. 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 post amputation, 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) .


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