PUBLICATION

Bifenthrin induces developmental immunotoxicity and vascular malformation during zebrafish embryogenesis

Authors
Park, S., Lee, J.Y., Park, H., Song, G., Lim, W.
ID
ZDB-PUB-191118-3
Date
2019
Source
Comparative biochemistry and physiology. Toxicology & pharmacology : CBP   228: 108671 (Journal)
Registered Authors
Keywords
Angiogenesis, Bifenthrin, Development, Embryotoxicity, Zebrafish
MeSH Terms
  • Animals
  • Cytokines/metabolism
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/immunology
  • Embryonic Development/drug effects*
  • Embryonic Development/immunology
  • Human Umbilical Vein Endothelial Cells/drug effects
  • Humans
  • Immune System/drug effects*
  • Insecticides/toxicity*
  • Models, Animal
  • Pyrethrins/toxicity*
  • Reactive Oxygen Species/metabolism
  • Receptors, Vascular Endothelial Growth Factor/metabolism
  • Vascular Malformations/chemically induced*
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/embryology*
PubMed
31734314 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.
CTD
31734314
Abstract
Bifenthrin is a synthesized pyrethroid insecticide which is frequently used in the farmland to eradicate insects. Bifenthrin mainly disrupts sodium ion channel inducing neurotoxicity in the target insects. It also exerts toxic effects such as hormone dysregulation, hepatotoxicity and immunotoxicity in other vertebrates. However, there is no evidence of the acute-toxicity associated embryogenesis and organogenesis of bifenthrin in zebrafish. Here we first demonstrated that bifenthrin induced acute-toxicity accompanying inflammatory response and physiological degradations resulting in loss of embryogenesis and vascular development in zebrafish embryos. We found that bifenthrin increased intestinal ROS accumulation and the inflammatory genes including tnfa, il6, il8 and ptgs2b, thereby increasing embryo mortality. Moreover, bifenthrin disrupted angiogenesis by down-regulation of VEGF receptors in embryos. Not only in the zebrafish, bifenthrin also decreased cell viability and hampered vascular formation of HUVECs. Collectively, bifenthrin induced developmental toxicity, inflammatory cell death and anti-angiogenesis during embryogenesis.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping