PUBLICATION
Haloxyfop-P-methyl induces developmental defects in zebrafish embryos through oxidative stress and anti-vasculogenesis
- Authors
- Park, S., Lee, J.Y., Park, H., Song, G., Lim, W.
- ID
- ZDB-PUB-200422-118
- Date
- 2020
- Source
- Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 233: 108761 (Journal)
- Registered Authors
- Keywords
- Haloxyfop-P-methyl, Neurotoxicity, Oxidative stress, Vasculogenesis, Zebrafish
- MeSH Terms
-
- Animals
- Embryo, Nonmammalian/drug effects
- Embryonic Development/drug effects*
- Herbicides/toxicity
- Neovascularization, Physiologic/drug effects*
- Oxidative Stress/drug effects*
- Pyridines/toxicity*
- Water Pollutants, Chemical/toxicity
- Zebrafish/embryology*
- PubMed
- 32289526 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.
Citation
Park, S., Lee, J.Y., Park, H., Song, G., Lim, W. (2020) Haloxyfop-P-methyl induces developmental defects in zebrafish embryos through oxidative stress and anti-vasculogenesis. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 233:108761.
Abstract
Haloxyfop-P-methyl, an aryloxyphenoxypropionate herbicide, is widely used to eliminate unwanted plants by inhibiting lipid synthesis and inducing oxidative stress. Since haloxyfop-P-methyl targets are limited within plants, few negative side effects on non-target crops have been reported. However, dissolved haloxyfop-P-methyl in rain or groundwater contaminates aquatic environments and affects marine ecosystems. In the present study, treatment with haloxyfop-P-methyl for 48 h induced developmental deficiencies in the eyes and bodies of the zebrafish embryos as a whole and was also linked to increases in the incidence of pericardial edema. Additionally, haloxyfop-P-methyl treatment decreased hatching ratio, embryo viability, and heart rate, while simultaneously increasing the expression levels of apoptotic and inflammatory genes. Moreover, haloxyfop-P-methyl hampered vasculogenesis in the embryos through down-regulation of functional genes, and disruption of vessel formation caused neurodegeneration in the olig2-positive notochord. Collectively, this study newly discovered the oxidative stress-related toxic mechanism of haloxyfop-P-methyl during embryonic development through anti-vasculogenesis, which suppresses neurogenesis of the notochord. This toxicity assessment of haloxyfop-P-methyl on embryogenesis may contribute to establishment of safety profiling of herbicide and to support hazard control in aquatic environment.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping