Abstract
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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