Bixafen exposure induces developmental toxicity in zebrafish (Danio rerio) embryos.

ABSTRACT

Bixafen (BIX), a new generation succinate dehydrogenase inhibitor (SDHI) fungicide commonly used in agriculture, is regarded as a potential aquatic pollutant because of its lethal and teratogenic effects on Xenopus tropicalis embryos. To evaluate the threat of BIX to aquatic environments, information concerning BIX's embryonic toxicity to aquatic organisms (especially fish) is important, yet such information remains scarce. The present study aimed to fill this knowledge gap by employing zebrafish embryos as model animals in exposure to 0.1, 0.3 and 0.9 µM BIX. Our results showed that BIX caused severe developmental abnormalities (hypopigmentation, tail deformity, spinal curvature and yolk sac absorption anomaly) and hatching delay in zebrafish embryos. The expression levels of early embryogenesis-related genes (gh, crx, sox2 and neuroD) were downregulated after BIX exposure, except for nkx2.4b, which was upregulated. Furthermore, transcriptome sequencing analysis showed that all the downregulated differentially expressed genes were enriched in cell cycle processes. Taken together, these results demonstrated that BIX has strong developmental toxicity to zebrafish that may be due to the downregulated expression of genes involved in embryonic development. These findings provide valuable reference for evaluating BIX's potential adverse effects on aquatic ecosystems.