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

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.

• Authors: Jin-Young Lee, Hahyun Park, Whasun Lim, Gwonhwa Song
• Journal: The Science of the total environment (Sci Total Environ) Vol. 771 Pg. 145445 (Jun 01 2021) ISSN: 1879-1026 [Electronic] Netherlands
• PMID: 33548715 (Publication Type: Journal Article)
• Copyright: Copyright © 2021 Elsevier B.V. All rights reserved.

Chemical References

• Aniline Compounds
• aclonifen

Topics

• Aniline Compounds
• Animals
• Embryo, Nonmammalian
• Embryonic Development
• Mitochondria (metabolism)
• Oxidative Stress
• Zebrafish