PUBLICATION

Exposure to Oxadiazon-Butachlor causes cardiac toxicity in zebrafish embryos

Authors
Huang, Y., Ma, J., Meng, Y., Wei, Y., Xie, S., Jiang, P., Wang, Z., Chen, X., Liu, Z., Zhong, K., Cao, Z., Liao, X., Xiao, J., Lu, H.
ID
ZDB-PUB-200607-7
Date
2020
Source
Environmental pollution (Barking, Essex : 1987)   265: 114775 (Journal)
Registered Authors
Lu, Huiqiang
Keywords
Cardiotoxicity, Oxadiazon-butachlor, Oxidative stress, WNT signaling Pathway, Zebrafish
MeSH Terms
  • Acetanilides
  • Animals
  • Cardiotoxicity*
  • Embryo, Nonmammalian
  • Oxadiazoles
  • Oxidative Stress
  • Zebrafish*
PubMed
32504889 Full text @ Environ. Pollut.
CTD
32504889
Abstract
Oxadiazon-Butachlor (OB) is a widely used herbicide for controlling most annual weeds in rice fields. However, its potential toxicity in aquatic organisms has not been evaluated so far. We used the zebrafish embryo model to assess the toxicity of OB, and found that it affected early cardiac development and caused extensive cardiac damage. Mechanistically, OB significantly increased oxidative stress in the embryos by inhibiting antioxidant enzymes that resulted in excessive production of reactive oxygen species (ROS), eventually leading to cardiomyocyte apoptosis. In addition, OB also inhibited the WNT signaling pathway and downregulated its target genes includinglef1, axin2 and β-catenin. Reactivation of this pathway by the Wnt activator BML-284 and the antioxidant astaxanthin rescued the embryos form the cardiotoxic effects of OB, indicating that oxidative stress, and inhibition of WNT target genes are the mechanistic basis of OB-induced damage in zebrafish. Our study shows that OB exposure causes cardiotoxicity in zebrafish embryos and may be potentially toxic to other aquatic life and even humans.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping