PUBLICATION
Exposure to diclofop-methyl induces cardiac developmental toxicity in zebrafish embryos
- Authors
- Cao, Z., Huang, Y., Xiao, J., Cao, H., Peng, Y., Chen, Z., Liu, F., Wang, H., Liao, X., Lu, H.
- ID
- ZDB-PUB-200115-15
- Date
- 2020
- Source
- Environmental pollution (Barking, Essex : 1987) 259: 113926 (Journal)
- Registered Authors
- Lu, Huiqiang
- Keywords
- Cardiotoxicity, Diclofop-methyl, Oxidative stress, Wnt, Zebrafish
- MeSH Terms
-
- Animals
- Embryo, Nonmammalian
- Halogenated Diphenyl Ethers/toxicity*
- Heart/drug effects
- Heart/growth & development*
- Herbicides/toxicity*
- Oxidative Stress
- Zebrafish/embryology*
- Zebrafish Proteins
- PubMed
- 31935613 Full text @ Environ. Pollut.
- CTD
- 31935613
Citation
Cao, Z., Huang, Y., Xiao, J., Cao, H., Peng, Y., Chen, Z., Liu, F., Wang, H., Liao, X., Lu, H. (2020) Exposure to diclofop-methyl induces cardiac developmental toxicity in zebrafish embryos. Environmental pollution (Barking, Essex : 1987). 259:113926.
Abstract
Diclofop-methyl (DM) is one of the most widely used herbicides in agriculture production and has been frequently detected in both freshwater and environments, even agricultural products. However, the potential toxic effects of DM on organisms and the underlying mechanisms are still poorly understood. In this study, we utilized zebrafish to evaluate the toxicity of DM during the cardiovascular developmental process. Exposure of zebrafish embryos to 0.75, 1.0 and 1.25 mg/L DM induced cardiac defects, such as pericardial edema, slow heart rate and long SV-BA distance but the vascular development in zebrafish larvae was not influenced by DM treatment. The expression of cardiac-related genes were disordered and DM exposure initiated disordering cardiogenesis from the period of precardiac mesoderm formation. Moreover, the apoptosis and proliferation of cardiomyocytes were not influenced but the levels of oxidative stress were upregulated by DM exposure. Fullerenes and astaxanthin was able to rescue cardiac defects caused by DM via downregulating oxidative stress. Wnt signaling was downregulated after DM treatment and activation of Wnt signaling could rescue cardiac defects. Therefore, our results suggest that DM has the potential to induce cardiac developmental toxicity through upregulation of Wnt-Mediated (reactive oxygen species) ROS generation in zebrafish larvae.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping