Abstract
Abamectin is an insecticide, miticide and nematicide that has been extensively used in agriculture for many years. The excessive use of abamectin inevitably pollutes water and soil and might even cause adverse effects on aquatic biota. However, it is currently unclear how abamectin exposure causes neurotoxicity in aquatic organisms. Herein, the early neural system development was assessed in zebrafish embryos following abamectin exposure. After treatment with a concentration gradient of abamectin (0.055, 0.0825, 0.11 mg/L), the survival rate, average heart rate, pericardial edema area and yolk sac edema were all documented in zebrafish embryos (96 hpf). It was found that after abamectin exposure, embryonic brain development was impaired, and motor behaviors were also affected. The fluorescence intensity was reduced in the transgenic embryos (Eno2: GFP). The activities of acetylcholinesterase (AChE) and ATPase were decreased, and the expression of neurodevelopment-related genes, such as sox10, gap43, grin1b, abat, gad1b, grin2b, nestin and glsa, were all inhibited in zebrafish embryo treatment with abamectin. Furthermore, the reactive oxygen species (ROS) were triggered upon exposure to abamectin in zebrafish embryos along with the accumulation of ROS, eventually resulting in neuroapoptosis in the developing embryonic brain. In conclusion, neurodevelopmental toxicity was caused by oxidative stress-induced apoptosis in zebrafish embryos following abamectin exposure.