Aclonifen causes developmental abnormalities in zebrafish embryos through mitochondrial dysfunction and oxidative stress

Jin Young Lee, Hahyun Park, Whasun Lim, Gwonhwa Song

Research output: Contribution to journalArticlepeer-review

Abstract

The herbicide aclonifen is commonly used in agriculture. Aclonifen is toxic to experimental animals, causing developmental abnormalities, decreased energy production for survival, and impaired organogenesis. However, no studies have reported the functional defects and toxicity caused by aclonifen in embryonic development. We hypothesized that the mechanism underlying the toxicity of several herbicides in various organisms involves mitochondrial dysfunction, which subsequently promotes genotoxicity, cytotoxicity, and acute organotoxicity. In the present study, we demonstrated that mitochondrial dysfunction during development results in decreased body length, delayed yolk sac absorption, malformed spinal cord, disrupted brain and eye formation, and the activation of apoptosis in zebrafish embryos. Aclonifen induced oxidative stress by elevating the level of reactive oxygen species, causing mitochondrial damage. Likewise, impaired embryonic vascularization can promote cardiovascular disorders. In this study, we characterized the toxicity of aclonifen in a non-target organism. These findings increase our understanding of the toxicological effects of herbicides in unexpected environments.

Original languageEnglish
Article number145445
JournalScience of the Total Environment
Volume771
DOIs
Publication statusPublished - 2021 Jun 1

Keywords

  • Aclonifen
  • Development inhibition
  • Mitochondrial dysfunction
  • Toxicological mechanism
  • Vasculature disruption
  • Zebrafish

ASJC Scopus subject areas

  • Environmental Engineering
  • Environmental Chemistry
  • Waste Management and Disposal
  • Pollution

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