TY - JOUR
T1 - Bifenthrin induces developmental immunotoxicity and vascular malformation during zebrafish embryogenesis
AU - Park, Sunwoo
AU - Lee, Jin Young
AU - Park, Hahyun
AU - Song, Gwonhwa
AU - Lim, Whasun
N1 - Funding 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 ).
PY - 2020/2
Y1 - 2020/2
N2 - 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.
AB - 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.
KW - Angiogenesis
KW - Bifenthrin
KW - Development
KW - Embryotoxicity
KW - Zebrafish
UR - http://www.scopus.com/inward/record.url?scp=85075002924&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85075002924&partnerID=8YFLogxK
U2 - 10.1016/j.cbpc.2019.108671
DO - 10.1016/j.cbpc.2019.108671
M3 - Article
C2 - 31734314
AN - SCOPUS:85075002924
VL - 228
JO - Comparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology
JF - Comparative Biochemistry and Physiology Part - C: Toxicology and Pharmacology
SN - 1532-0456
M1 - 108671
ER -