Acetamiprid-induced Cyto- and Genotoxicity in the AR42J Pancreatic Cell Line.

Abstract

Neonicotinoid insecticides, 30% of insecticides marketed worldwide, have selective toxicity on insects through α4p2 nicotinic acetylcholine receptors. Although it is known that acetamiprid exerts toxicity on several organ systems, its toxic effects on the pancreas and its mechanism of action have not been clarified yet. Therefore, in the present study, the cytotoxic and genotoxic potentials of acetamiprid on the AR42J pancreatic cell line were evaluated. The (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) (MTT) assay and comet assay were conducted for the cyto- and genotoxicity evaluations, respectively. Reactive oxygen species (ROS) production was assessed by flow cytometry and glutathione (GSH) levels were determined by ELISA for oxidative damage potential, which is thought to be an underlying mechanism of cyto-/genotoxic effects. To reveal the dose-response relationship the concentration range of 1-6 mM was selected for the assays. Cell viability decreased in a dose-dependent manner and the inhibitory concentration 50 value was calculated as 12.61 mM by the MTT assay. Acetamiprid induced DNA damage in all concentrations tested in a dose-depending manner. The mean tail intensity values were 3.84 and ≤32.96 for the control and exposure groups, respectively. There was no significant difference for ROS production; however, the GSH level was reduced at the highest concentration. It is thought that the present study will contribute to the literature due to the lack of data on the potential toxic effects of acetamiprid on the pancreas. To better understand acetamiprid toxicity, further studies including a wide range of mechanistic parameters are needed.