Fluxapyroxad induces developmental delay in zebrafish (Danio rerio).

Succinate dehydrogenase inhibitor (SDHI) fungicides are extensively used in agriculture. Some SDHI fungicides show developmental toxicity, immune toxicity and hepatotoxicity to fish. Fluxapyroxad (FLU) is a broad spectrum pyrazole-carboxamide SDHI fungicide and its potential impacts on fish embryonic development are unknown. We exposed zebrafish embryos to 1, 2 and 4 μM FLU. Developmental malformations, including yolk sac absorption disorder, decreased pigmentation and hatch delay were induced after FLU exposure. FLU caused significantly increased transcription levels in the ectoderm marker foxb1a but no significant changes in endoderm and mesoderm development markers (foxa2, ntl and eve1). Transcription levels of genes in the early stage embryos (gh, crx, neuroD and nkx2.4b) decreased significantly after FLU treatments. The content of glutathione (GSH) increased after FLU exposure. This study shows that FLU is toxic to zebrafish through its developmental effects and oxidative stress. FLU may pose risks to other non-target aquatic organisms.