PUBLICATION

2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibits zebrafish caudal fin regeneration

Authors
Zodrow, J.M. and Tanguay, R.L.
ID
ZDB-PUB-030826-17
Date
2003
Source
Toxicological sciences : an official journal of the Society of Toxicology   76(1): 151-161 (Journal)
Registered Authors
Tanguay, Robyn L., Zodrow, Jean
Keywords
none
MeSH Terms
  • Animals
  • Aryl Hydrocarbon Hydroxylases/biosynthesis
  • Aryl Hydrocarbon Receptor Nuclear Translocator
  • Cell Division/drug effects
  • DNA-Binding Proteins*
  • Dose-Response Relationship, Drug
  • Extremities/anatomy & histology
  • Extremities/physiology
  • Receptors, Aryl Hydrocarbon/biosynthesis
  • Regeneration/drug effects*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription Factors/biosynthesis
  • Zebrafish/metabolism
  • Zebrafish/physiology*
  • Zebrafish Proteins/biosynthesis
PubMed
12915709 Full text @ Toxicol. Sci.
CTD
12915709
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.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping