Pyrimethanil is a broad-spectrum fungicide commonly used in the prevention and treatment of Botrytis cinerea. However, little information is available in the literature to show the toxicity of
Pyrimethanil to cardiac development. In this study, we used an experimental animal model to explore the developmental and
cardiac toxicity of
Pyrimethanil in aquatic vertebrates; we exposed zebrafish embryos to
Pyrimethanil at concentrations of 2, 4, and 6 mg/L from 5.5 to 72 h post fertilisation. We found that
Pyrimethanil caused a decrease in the hatching rate, heart rate, and survival rate of zebrafish embryos.
Pyrimethanil exposure also resulted in pericardial and yolk sac
edema, spinal
deformity, and heart loop failure. Moreover,
Pyrimethanil increased reactive
oxygen stress levels and heightened the activity of
superoxide dismutase and
catalase. Alterations were induced in the transcription of apoptosis-related genes (p53, Bax, Bcl2, Casp 9, and Casp6l1) and heart development-related genes (Tbx2b, Gata4, Myh6, Vmhc,
Nppa, Bmp2b, Bpm 4, and Bpm 10). Our data showed that the activation of Wnt signalling by BML-284 could partially rescue the malformed phenotype caused by
Pyrimethanil. Our results provide new evidence for
Pyrimethanil's toxicity and the danger of its residues in the environment and agricultural products.