The involvement of ROS generation on Epoxiconazole-induced toxicity in HCT116 cells

Triazole fungicides are the most efficient class of pesticides and have been in rapid development since the 1970s, receiving worldwide recognition. Epoxiconazole is a systemic fungicide belonging to the most widely used members of triazole group and its environmental residue in water has been detected at concentrations up to 7.7 g/l [1]. However, there is few information regarding the molecular mechanism by which EPX exerts its cytotoxic and genotoxic effects. The present study aims to investigate the toxic effects of EPX in human colon carcinoma cell line (HCT116). We demonstrated that EPX significantly decreased cell viability as assessed by the MTT assay. The increase in cell death was accompanied by a reduction in the mitochondrial membrane potential. In addition, we have shown that EPX induced the generation of reactive oxygen species (ROS) and therefore increased the lipid peroxidation as evidenced by the high levels of MDA. Moreover, our results indicate that EPX induced a concentration-dependent increase in DNA damage as evident by the Comet assay. More interestingly, the induction of cell mortality was attenuated when cells were pretreated with the antioxidant; N-acetylcysteine (NAC) indicating that ROS generation plays a crucial role in the induction of cell death by EPX.