Oxidative stress mediated cytotoxicity of tin (IV) oxide (SnO) nanoparticles in human breast cancer (MCF-7) cells.

Due to unique optical and electronic properties tin oxide nanoparticles (SnO NPs) have shown potential for various applications including solar cell, catalyst, and biomedicine. However, there is limited information concerning the interaction of SnO NPs with human cells. In this study, we explored the potential mechanisms of cytotoxicity of SnO NPs in human breast cancer (MCF-7) cells. Results demonstrated that SnO NPs induce cell viability reduction, lactate dehydrogenase leakage, rounded cell morphology, cell cycle arrest and low mitochondrial membrane potential in dose- and time-dependent manner. SnO NPs were also found to provoke oxidative stress evident by generation of reactive oxygen species (ROS), hydrogen peroxide (HO) and lipid peroxidation, while depletion of glutathione (GSH) level and lower activity of several antioxidant enzymes. Remarkably, we observed that ROS generation, GSH depletion, and cytotoxicity induced by SnO NPs were effectively abrogated by antioxidant N-acetylcycteine. Our data have shown that SnO NPs induce toxicity in MCF-7 cells via oxidative stress. This study warrants further research to explore the genotoxicity of SnO NPs in different types of cancer cells.