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.
|Journal||Comparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology|
|Publication status||Published - 2020 Feb|
Bibliographical noteFunding Information:
This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute funded by the Ministry of Health and Welfare (grant number: HI17C0929 ) and the National Research Foundation of Korea (NRF) grant funded by the Ministry of Science and ICT (MSIT) (No. 2018R1C1B6009048 ).
© 2019 Elsevier Inc.
ASJC Scopus subject areas
- Cell Biology
- Health, Toxicology and Mutagenesis