Oxidative stress mediated cytotoxicity and apoptosis response of bismuth oxide (Bi2O3) nanoparticles in human breast cancer (MCF-7) cells.

Bismuth oxide nanoparticles (Bi2O3 NPs) have shown great potential for several applications including cosmetics and biomedicine. However, there is paucity of research on toxicity of Bi2O3 NPs. In this study, we first examined dose-dependent cytotoxicity and apoptosis response of Bi2O3 NPs in human breast cancer (MCF-7) cells. We further explored the potential mechanisms of cytotoxicity of Bi2O3 NPs through oxidative stress. Physicochemical study demonstrated that Bi2O3 NPs have crystalline structure and spherical shape with mean size of 97 nm. Toxicity studies have shown that Bi2O3 NPs reduce cell viability and induce membrane damage dose-dependently in the concentration range of 50-300 μg/ml. Bi2O3 NPs also disturbed cell cycle of MCF-7 cells. Oxidative stress response of Bi2O3 NPs was evident by generation of reactive oxygen species (ROS), higher lipid peroxidation, reduction of glutathione (GSH) and low superoxide dismutase (SOD) enzyme activity. Interestingly, supplementation of external antioxidant N-acetyl-cysteine almost negated the effect of Bi2O3 NPs induced oxidative stress and cell death. We also found that exposure of Bi2O3 NPs induced apoptotic response in MCF-7 cells suggested by impaired regulation of Bcl-2, Bax and caspase-3 genes. Altogether, we found that Bi2O3 NPs induced cytotoxicity in MCF-7 cells through modulating the redox homeostasis via Bax/Bcl-2 pathway. This study warranted further research to delineate the underlying mechanism of Bi2O3 NPs induced toxicity at in vivo level.