Induction of Developmental Toxicity and Cardiotoxicity in Zebrafish Embryos by Emamectin Be Nzoatethrough Oxidative Stress

Abstract

Emamectin benzoate (EMB) is a widely used pesticide in agriculture, but its potential risks to the environment and organisms have been overlooked. In this study, we evaluated the developmental toxicity cardiotoxicity of EMB using zebrafish model. We exposed zebrafish embryos to EMB of 0.5, 1.0, 1.5 and 2 μg/mL. We found that EMB caused mortality and abnormalities, such as pericardial edema, yolk sac edema, and spinal curvature and tail malformation. EMB exposure also resulted in oxidative stress, disruption of lipid metabolism and apoptosis. Moreover, EMB exposure caused abnormalities in zebrafish heart morphology and function, such as long SV-BA distance, pericardial edema, slow red blood cell flow rate 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 EMB induces developmental toxicity and cardiotoxicity in zebrafish. Our research provides new evidence on the environmental and organism effects of Emamectin benzoate.

Keywords: Emamectin benzoate, Developmental toxicity, oxidative stress, Cardiotoxicity, Zebrafish