Effects of embryonic exposure to fluxapyroxad on zebrafish (Danio rerio) ocular development

被引:11
|
作者
Qiu, Tiantong [1 ]
Chen, Xin [1 ]
Xiao, Peng [2 ]
Wang, Liqiang [1 ]
Li, Wenhua [1 ]
机构
[1] Huaqiao Univ, Engn Res Ctr Mol Med,Sch Biomed Sci, Minist Educ,Key Lab Precis Med & Mol Diag Fujian, Key Lab Fujian Mol Med,Key Lab Xiamen Marine & Ge, Xiamen 361021, Peoples R China
[2] Wenzhou Univ, Coll Life & Environm Sci, Wenzhou 325035, Zhejiang, Peoples R China
关键词
Fluxapyroxad; Zebrafish; Embryo; Retina; Apoptosis; DEHYDROGENASE-INHIBITOR FUNGICIDES; PHOTORECEPTOR DEVELOPMENT; INTRAOCULAR-PRESSURE; ENVIRONMENTAL FATE; SURFACE-WATER; CELL GENESIS; ROD; EXPRESSION; APOPTOSIS; MICROPHTHALMIA;
D O I
10.1016/j.pestbp.2021.105018
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Fluxapyroxad (FLU) is a succinate dehydrogenase inhibitor that protects crops from fungal diseases, however, it has been identified as toxicants to aquatic organisms. The objective of this study is to investigate the potential toxicity and underlying mechanisms of FLU on aquatic organisms. Herein, by using zebrafish embryos as a model organism, we demonstrated that FLU can cause microphthalmia in zebrafish embryos. The cell density in ganglion cell layer (GCL) is increased after exposure. Compared with the control, differentiation of the cells in ganglion cell layer, inner nuclear layer (INL), and outer nuclear layer (ONL) were severely disrupted in response to FLU treatment. The data show clear evidence that FLU exhibits development toxicity to zebrafish embryos by inducing retinal cell apoptosis, which causes microphthalmia. Our study provides comprehensive understanding to the underlying mechanism of FLU toxicity.
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页数:8
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