Mechanism of cell death induced by silica nanoparticles in hepatocyte cells is by apoptosis

Silicon is one of the most widely used chemical materials, and the increasing use of silica nanoparticles (SNs) highlights the requirement for safety and biological toxicity studies. The damaging and adverse effects of SNs on human hepatocytes remain largely unknown, as do the mechanisms involved. In the present study, the mechanisms underlying SN-induced toxicity in the human hepatocyte cell line HL-7702 were investigated. An MTT assay revealed that following exposure to SNs in the concentration range of 25-200 µg/ml, the viability of HL-7702 cells decreased, and the viability decreased further with increasing exposure time. SNs induced a delay in the S and G2/M phases of the cell cycle, and also induced DNA damage in these cells. Western blot and flow cytometry analyses revealed that cell death was mediated by mitochondrial damage and the upregulated expression of a number of pro-apoptotic proteins. In conclusion, exposure to SNs led to mitochondrial and DNA damage, resulting in apoptosis-mediated HL-7702 cell death. The study provided evidence for the cellular toxicity of SNs, and added to the growing body of evidence regarding the potential damaging effects of nanoparticles, indicating that caution should be exercised in their widespread usage.