Neonicotinoids are a group of pesticides widely used in agriculture and at home. Among those pesticides, acetamiprid (ACM) is a broad-spectrum insecticide used for the protection of vegetables and fruits from pest. The extensive use of this pesticide had led to contamination of environment including soil, water, as well as food products. However, there are few informations regarding the molecular mechanism by which ACM exerts its cytotoxic and genotoxic effects. The aim of the present study was to investigate the toxic effects of ACM in PC12 cells. We demonstrated that ACM significantly decreased cell viability as assessed by the MTT assay. We also shown that ACM-induced reactive oxygen species (ROS) generation followed by lipid peroxidation as evidenced by an increase in the MDA levels. The increase in cell death was accompanied by a reduction in the mitochondrial membrane potential. Besides, pretreatment with Z-VAD-FMK, a general caspases inhibitor, significantly decreased the ACM-induced cell death. Our results also indicate that ACM induced a concentration-dependent increase in DNA damage as evident by the Comet assay. These data indicate that ACM produces cytotoxicity and DNA damage in mammalian cells. Highlights ACM is cytotoxic toward rat pheochromocytoma adrenal medulla cells (PC12). ACM induces ROS generation, lipid peroxidation, and DNA fragmentation. ACM induces caspase-dependent apoptosis in PC12 cells.
Keywords: Acetamiprid; DNA fragmentation; PC12; apoptosis; oxidative stress.