Dimethenamid promotes oxidative stress and apoptosis leading to cardiovascular, hepatic, and pancreatic toxicities in zebrafish embryo

Junho Park, Garam An, Jeankyoung You, Hahyun Park, Taeyeon Hong, Gwonhwa Song, Whasun Lim

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Dimethenamid, one of the acetamide herbicides, is widely used on soybeans and corns to inhibit weed growth. Although other acetamide herbicides have been reported to have several toxicities in non-target organisms including developmental toxicity, the toxicity of dimethenamid has not yet been studied. In this research, we utilized the zebrafish animal model to verify the developmental toxicity of dimethenamid. It not only led to morphological abnormalities in zebrafish larvae but also reduced their viability. ROS production and inflammation responses were promoted in zebrafish larvae. Also, uncontrolled apoptosis occurred when the gene expression level related to the cell cycle and apoptosis was altered by dimethenamid. These changes resulted in toxicities in the cardiovascular system, liver, and pancreas are observed in transgenic zebrafish models including fli1a:EGFP and L-fabp:dsRed;elastase:GFP. Dimethenamid triggered morphological defects in the heart and vasculature by altering the mRNA levels related to cardiovascular development. The liver and pancreas were also damaged through not only the changes of their morphology but also through the dysregulation in their function related to metabolic activity. This study shows the developmental defects induced by dimethenamid in zebrafish larvae and the possibility of toxicity in other non-target organisms.

Original languageEnglish
Article number109741
JournalComparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology
Volume273
DOIs
Publication statusPublished - 2023 Nov

Bibliographical note

Funding Information:
This research was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (grant number: 2021R1A2C2005841 ). This research was also supported by the Health Fellowship Foundation . This research was supported by Basic Science Research Program through the NRF funded by the Ministry of Education (grant number: 2019R1A6A1A10073079 ).

Publisher Copyright:
© 2023 Elsevier Inc.

Keywords

  • Apoptosis
  • Dimethenamid
  • Organ defects
  • Oxidative stress
  • Zebrafish model

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Aquatic Science
  • Animal Science and Zoology
  • Toxicology
  • Cell Biology
  • Health, Toxicology and Mutagenesis

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