Amisulbrom (AML), a sulfonamide fungicide used to control oomycete diseases, is regarded as a threat to aquatic species. The objective of this study was to evaluate the potential effects of AML on fish using a zebrafish model. Zebrafish embryos were exposed to 0.0075 μM, 0.075 μM, and 0.75 μM AML. AML-treated zebrafish embryos exhibited severe developmental defects, including pericardial edema, blood-clot clustering, increased hatching rates, decreased heart rates, and abnormal hemoglobin distributions. Compared with controls, key marker genes associated with cardiovascular development (i.e., nkx2.5, myh6, myh7, myl7, alas2, hbbe1, hbbe2, and gata1a) were abnormally expressed in response to AML treatment, suggesting that AML might specifically affect cardiovascular development. These results provide a valuable reference for the effects of AML on zebrafish embryos and may help to further clarify the potential risks posed by AML to aquatic ecosystems.
Keywords: Amisulbrom; Cardiovascular toxicity; Embryo; Gene expression; Zebrafish.
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