1. Academic Validation
  2. Haloxyfop-P-methyl induces developmental defects in zebrafish embryos through oxidative stress and anti-vasculogenesis

Haloxyfop-P-methyl induces developmental defects in zebrafish embryos through oxidative stress and anti-vasculogenesis

  • Comp Biochem Physiol C Toxicol Pharmacol. 2020 Jul;233:108761. doi: 10.1016/j.cbpc.2020.108761.
Sunwoo Park 1 Jin-Young Lee 2 Hahyun Park 1 Gwonhwa Song 3 Whasun Lim 4
Affiliations

Affiliations

  • 1 Institute of Animal Molecular Biotechnology and Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea.
  • 2 Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
  • 3 Institute of Animal Molecular Biotechnology and Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea. Electronic address: ghsong@korea.ac.kr.
  • 4 Department of Food and Nutrition, Kookmin University, Seoul 02707, Republic of Korea. Electronic address: wlim@kookmin.ac.kr.
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.

Keywords

Haloxyfop-P-methyl; Neurotoxicity; Oxidative stress; Vasculogenesis; Zebrafish.

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