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

Bismuth oxide nanoparticles (BiO NPs) have shown great potential for several applications including cosmetics and biomedicine. However, there is paucity of research on toxicity of BiO NPs. In this study, we first examined dose-dependent cytotoxicity and apoptosis response of BiO NPs in human breast cancer (MCF-7) cells. We further explored the potential mechanisms of cytotoxicity of BiO NPs through oxidative stress. Physicochemical study demonstrated that BiO NPs have crystalline structure and spherical shape with mean size of 97 nm. Toxicity studies have shown that BiO NPs reduce cell viability and induce membrane damage dose-dependently in the concentration range of 50-300 μg/ml. BiO NPs also disturbed cell cycle of MCF-7 cells. Oxidative stress response of BiO 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 BiO NPs induced oxidative stress and cell death. We also found that exposure of BiO NPs induced apoptotic response in MCF-7 cells suggested by impaired regulation of Bcl-2, Bax and caspase-3 genes. Altogether, we found that BiO 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 BiO NPs induced toxicity at in vivo level.