PUBLICATION

Picolinafen exerts developmental toxicity via the suppression of oxidative stress and angiogenesis in zebrafish embryos

Authors
Lee, J.Y., Park, S., Lim, W., Song, G.
ID
ZDB-PUB-201229-14
Date
2021
Source
Pesticide biochemistry and physiology   171: 104734 (Journal)
Registered Authors
Keywords
Angiogenesis, Developmental toxicity, Oxidative stress, Picolinafen, Zebrafish
MeSH Terms
  • Animals
  • Apoptosis
  • Embryo, Nonmammalian
  • Herbicides*/toxicity
  • Oxidative Stress
  • Reactive Oxygen Species
  • Water Pollutants, Chemical*
  • Zebrafish
PubMed
33357556 Full text @ Pestic Biochem Physiol
Abstract
Picolinafen, a phytoene desaturase-inhibiting herbicide, has been used since 2001 to control the growth of broadleaf weeds. Picolinafen has lower solubility and volatility, and shows lower toxicity to non-target insect species than other types of herbicide. Although picolinafen has been detected in lakes near urban environments and induces chronic toxicity in the mammals, birds, and some aquatic organisms, no study has investigated the toxicity or mode of action of picolinafen in zebrafish. In this study, we demonstrated the lethality and acute LC50 value of picolinafen towards zebrafish embryos. Picolinafen hampered the development of embryos by the induction of morphological abnormalities via apoptosis. Additionally, picolinafen suppressed the generation of reactive oxygen species and angiogenesis. Also, the angiogenesis related genes, flt1 and flt4 mRNA expression was decreased in zebrafish embryos. This study provides a mechanistic understanding of the developmental toxicity of picolinafen in vertebrates.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping