Toxic effects and potential mechanisms of Fluxapyroxad to zebrafish (Danio rerio) embryos

Fluxapyroxad is a broad-spectrum and high-efficiency succinate dehydrogenase inhibitor fungicide that can control plant fungal pathogens on many crops. However, fluxapyroxad can enter the aquatic environment when applied in the field, which has an impact on the aquatic environment. The potential threat and toxicological mechanisms of fluxapyroxad in aquatic organisms remain poorly understood. In this study, zebrafish embryos were exposed to fluxapyroxad to investigate the toxic effects and potential mechanisms of fluxapyroxad. In the acute toxicity test, the lethal sensitivity rank of the zebrafish during the three stages was larvae (0.699 mg/L) > adult fish (0.913 mg/L) > embryo (1.388 mg/L). Fluxapyroxad induced abnormal spontaneous movement, malformations and decreased heartbeat, hatching percentage, and body length of the embryos. In the sublethal toxicity test, succinate dehydrogenase activity was significantly increased in all treatment groups, while the activities of the electron transport chain complex II and ATPase were markedly inhibited in 0.347 and 0.694 mg/L fluxapyroxad groups compared to that of the control group. Exposure to fluxapyroxad resulted in significant increases in MDA production, and GPx activity was significantly reduced at 0.694 mg/L. Moreover, caspase-3 activity was significantly increased in the 0.694 mg/L group, and the expression of the genes related to growth (bmp4 and lox) was inhibited after fluxapyroxad exposure. These results indicated that oxidative stress, cell apoptosis and mitochondrial damage might be the potential mechanism underlying the toxic effects of fluxapyroxad on zebrafish embryos. (C) 2021 Elsevier B.V. All rights reserved.

Automated summary

The study found that fluxapyroxad has toxic effects on zebrafish embryos, causing abnormal spontaneous movement, malformations, decreased heartbeat, and affecting key enzyme activities such as succinate dehydrogenase. Oxidative stress, cell apoptosis, and mitochondrial damage may be the toxic mechanisms.