Fluxapyroxad (FLU) is a succinate dehydrogenase inhibitor (SDHI) fungicide used in controlling crop diseases. Potential toxicity to aquatic organisms is not known. We exposed zebrafish to 1, 2, and 4 μM FLU for 3 days. The embryonic zebrafish showed developmental cardiac defects, including heart malformation, pericardial edema, and heart rate reduction. Compared with the controls, cardiac-specific transcription factors (nkx2.5, myh7, myl7, and myh6) exhibited dysregulated expression patterns after FLU treatment. We next used transcriptome and qRT-PCR analyses to explore the molecular mechanism of FLU cardiotoxicity. The transcriptome analysis and interaction network showed that the downregulated genes were enriched in calcium signaling pathways, adrenergic signaling in cardiomyocytes, and cardiac muscle contraction. FLU exposure repressed the cardio-related calcium signaling pathway, associated with apoptosis in the heart and other manifestations of cardiotoxicity. Thus, the findings provide valuable evidence that FLU exposure causes disruption of cardiac development in zebrafish embryos. Our findings will help to promote a better understanding of the toxicity mechanisms of FLU and act as a reference to explore the rational use and safety of FLU in agriculture.
Keywords: Cardiotoxicity; Embryo; Fluxapyroxad; Heart malformation; Transcriptome; Zebrafish.
© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.