Toxicity and oxidative damage of meperfluthrin on cardiac development of zebrafish embryos and larvae

Meperfluthrin is one of the top-selling sanitary insecticide species in the domestic market, drawing widespread attention due to its environmental safety risk. In this paper, zebrafish was used as an experimental model to assess the cardiac developmental toxicity and oxidative damage caused by acute exposure to meperfluthrin in embryos and larvae. The acute toxicity assessment revealed that meperfluthrin is highly toxic to zebrafish embryos with a 72 h-LC₅₀ of 0.756 μg/mL. After exposure to different doses of meperfluthrin (0, 0.2, 0.4, 0.8 μg/mL) for 72 h, the larvae from 0.4 and 0.8 μg/mL dose-treated groups showed deformities, including spine and tail curvature, pericardium and yolk sac edema, significant reduction of heart rate and hatchability, and incomplete embryonic development (shorter body length, smaller head, and eye area). Moreover, meperfluthrin of 0.2, 0.4, and 0.8 μg/mL induced atrial and ventricular differentiation in larvae, and down-regulated the expression of cardiac function-related genes myl7, myh6, and vmhc. It also increased the content of malondialdehyde (MDA), as well as decreased the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), resulting in the accumulation of reactive oxygen species (ROS) in the heart of larvae. The results of this paper indicate that meperfluthrin exposure has significant toxicity to the cardiac development of zebrafish embryos and is associated with oxidative damage.