PUBLICATION

Polychlorinated Diphenylsulfides Activate Aryl Hydrocarbon Receptor 2 in Zebrafish Embryos: Potential Mechanism of Developmental Toxicity

Authors
Zhang, R., Wang, X., Zhang, X., Song, C., Letcher, R.J., Liu, C.
ID
ZDB-PUB-180310-11
Date
2018
Source
Environmental science & technology   52(7): 4402-4412 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Gene Expression Regulation
  • Dioxins*
  • Receptors, Aryl Hydrocarbon
  • Zebrafish Proteins*
  • Animals
  • Animals, Genetically Modified
  • Zebrafish
PubMed
29522672 Full text @ Env. Sci. Tech.
Abstract
It is hypothesized that polychlorinated diphenyl sulfides (PCDPSs) induce lethal toxicity in zebrafish which is mediated by aryl hydrocarbon receptor 2 (Ahr2) activation. In this study an assay was developed based on in vivo exposure of wild-type and Tg(cyp1a:gfp) transgenic zebrafish embryos/larvae to PCDPS congeners (i.e. six dichloro- to heptachloro-diphenyl sulfides) coupled with a zebrafish Ahr2-luciferase reporter gene (LRG) expression. Waterborne PCDPSs were found to be accumulated in zebrafish larvae and exposure to PCDPSs led to a significant increase in mortality and cyp1s mRNA expression. Furthermore, treatment with PCDPSs caused a significant induction of Ahr2-LRG activity in COS-7 cells, and extremely significant correlations were observed between the in vivo median lethal concentrations and the levels of cyp1s mRNA expression and Ahr2 activation. Molecular dynamics simulations indicated the interaction between dioxins/dioxin-like compounds (DLCs) and six key amino acid residues in the ligand-binding domain of Ahr2 probably determined the susceptibility to dioxins/DLCs in zebrafish. These results strongly support the hypothesis that early life-stage mortality of zebrafish is initiated and mediated by Ahr2 activation.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping