Oxidative stress mediated cytotoxicity of tin (IV) oxide (SnO 2 ) nanoparticles in human breast cancer (MCF-7) cells

Abstract

Due to unique optical and electronic properties tin oxide nanoparticles (SnO 2 NPs) have shown potential for various applications including solar cell, catalyst, and biomedicine. However, there is limited information concerning the interaction of SnO 2 NPs with human cells. In this study, we explored the potential mechanisms of cytotoxicity of SnO 2 NPs in human breast cancer (MCF-7) cells. Results demonstrated that SnO 2 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 2 NPs were also found to provoke oxidative stress evident by generation of reactive oxygen species (ROS), hydrogen peroxide (H 2 O 2 ) 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 2 NPs were effectively abrogated by antioxidant N-acetylcycteine. Our data have shown that SnO 2 NPs induce toxicity in MCF-7 cells via oxidative stress. This study warrants further research to explore the genotoxicity of SnO 2 NPs in different types of cancer cells.