Induction of developmental toxicity and cardiotoxicity in zebrafish embryos by Emamectin benzoate through oxidative stress

Abstract

Emamectin benzoate (EMB) is a widely used pesticide in agriculture, but its potential risks to the environment and health have not been fully evaluated. In this study, we evaluated the toxicity of Emamectin benzoate using zebrafish model, and found that it affected early embryonic development, such as malformations and delayed hatching. Mechanistically, Emamectin benzoate increased oxidative stress by excessive production of reactive oxygen species (ROS) and abnormal activities of the antioxidant enzymes. Moreover, Emamectin benzoate exposure caused abnormalities in zebrafish heart morphology and function, such as long SV-BA distance and slow heart rate. Alterations were induced in the transcription of heart development-related genes (nkx2.5, tbx5, gata4 and myl7). In summary, our data showed that Emamectin benzoate induces developmental toxicity and cardiotoxicity in zebrafish. Our research provides new evidence on the Emamectin benzoate's toxicity and potential risk in human health.

Keywords: Cardiotoxicity; Developmental toxicity; Emamectin benzoate; Oxidative stress; Zebrafish.