Oxidative stress mediated cytotoxicity of tin (IV) oxide (SnO2) nanoparticles in human breast cancer (MCF-7) cells

[Display omitted] •We explored the cytotoxicity mechanism of SnO2 NPs in MCF-7 cells.•SnO2 NPs induced cytotoxicity in a dose and time-dependent manner.•SnO2 NPs induced ROS and H2O2 generation along with lipid peroxidation.•SnO2 NPs weakened the antioxidant capacity of cells.•SnO2 NPs induced cytotoxicity was found to be mediated through oxidative stress. Due to unique optical and electronic properties tin oxide nanoparticles (SnO2 NPs) have shown potential for various applications including solar cell, catalyst, and biomedicine. However, there is limited information concerning the interaction of SnO2 NPs with human cells. In this study, we explored the potential mechanisms of cytotoxicity of SnO2 NPs in human breast cancer (MCF-7) cells. Results demonstrated that SnO2 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. SnO2 NPs were also found to provoke oxidative stress evident by generation of reactive oxygen species (ROS), hydrogen peroxide (H2O2) 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 SnO2 NPs were effectively abrogated by antioxidant N-acetylcycteine. Our data have shown that SnO2 NPs induce toxicity in MCF-7 cells via oxidative stress. This study warrants further research to explore the genotoxicity of SnO2 NPs in different types of cancer cells.