Despite the widespread application of nickel nanoparticles (Ni NPs) in industrial, commercial, and biomedical fields, their response to human cells has not been clearly elucidated. In the study reported here, Ni NPs with a 28 nm diameter were used to study their interaction with human breast carcinoma (MCF-7) cells. Dose-dependent decreased cell viability and damaged cell membrane integrity showed the cytotoxic potential of the Ni NPs. We further found that Ni NPs induce oxidative stress in a dose-dependent manner, as evidenced by glutathione depletion and reactive oxygen species (ROS) generation. Comet assay indicated the dose-dependent induction of DNA damage due to Ni NP exposure. The level of messenger RNA, as well as activity of caspase-3 enzyme, was higher in MCF-7 cells exposed to Ni NPs than in control cells. Moreover, we observed statistically significant correlations of ROS with cell viability (R (2)=0.984), DNA damage (% tail DNA) (R (2)=0.982), and caspase-3 enzyme activity (R (2)=0.991). To the best of our knowledge, this is the first study on human breast cancer cells to have shown the cyto-genotoxicity of Ni NPs, which seems to be mediated through ROS.
Keywords: caspase-3 enzyme; cytotoxicity; genotoxicity; glutathione; reactive oxygen species.