Bismuth oxide nanoparticles induce oxidative stress and apoptosis in human breast cancer cells

Metal nanomaterials such as bismuth oxide nanoparticles (Bi(2)O(3)NPs) have been extensively used in cosmetics, dental materials, pulp capping, and biomedical imaging. There is little knowledge about the health risk of Bi(2)O(3)NPs in humans, which warrants a thorough toxicity investigation of Bi(2)O(3)NPs at the cellular level. In this experiment, we investigated the cytotoxic effect of Bi(2)O(3)NPs on human breast cancer (MCF-7) cells over 24 and 48 h. MCF-7 cells were exposed to Bi(2)O(3)NPs at varying doses (0.1, 0.5, 1.0, 5, 10, 20, 40 mu g/mL) for 24 and 48 h. We assessed the toxicity of Bi(2)O(3)NPs by measuring its effect on the viability and oxidative stress biomarkers, e.g., GSH, SOD, and catalase in MCF-7 cells. The pro-apoptotic effects of Bi(2)O(3)NPs on MCF-7 cells were determined via evaluating dysfunction of mitochondrial membrane potential (MMP), caspase-3 activity, externalization of phosphatidylserine, and chromosome condensation. Furthermore, apoptotic cells were evaluated using 7-AAD fluorescence stain and Annexin V-FITC. Bi(2)O(3)NPs induced oxidative stress in MCF-7 cells in a time- and dose-dependent manner. Bi(2)O(3)NPs increased the rate of both necrotic cells and apoptotic cells. In addition, the blue fluorescence of MCF-7 cells with condensed chromatin was increased in a time- and dose-dependent manner. In conclusion, the present study highlights the potential toxic effects of Bi(2)O(3)NPs at the cellular level and suggests further investigation of Bi(2)O(3)NPs before any medical purposes.

Automated summary

The experiment conducted on Bi(2)O(3)NPs revealed their ability to induce oxidative stress and increase apoptosis in human breast cancer cells, leading to dysfunction of mitochondrial membrane potential and chromosome condensation.