Research Article

Cytotoxicity and DNA damage in mouse macrophages exposed to silica nanoparticles

Published: August 30, 2016
Genet. Mol. Res. 15(3): gmr9005 DOI: 10.4238/gmr.15039005

Abstract

Silica (SiO2) nanoparticles are being progressively applied in various applications, including cosmetics, food technology, and medical diagnostics. Although crystalline SiO2 is a known carcinogen, the carcinogenicity of SiO2 nanoparticles remains unclear. Here, we assessed the cytotoxic effects and DNA injury induced by exposure to various dosages of SiO2 nanoparticles at 0-2400 mg/mL (0-3200 mg/mL microscale SiO2 as positive control) for 24 h using RAW264.7 cells, followed by methyl tetrazolium (MTT) assay. Cells were also treated by 31.25, 125, and 500 mg/mL SiO2 nanoparticles (500 mg/mL microscale SiO2 as positive control) for 24 h and examined by single cell gel electrophoresis assay (SCEG) and flow cytometry. Outstanding dose-related decline in cell viability was observed with enhancing dosages of SiO2 nanoparticles by MTT assay. The inhibitory concentration 50% of SiO2 nanoparticles and microscale SiO2 was 16690 and 5080 mg/mL, respectively. The comet rate (comet%), length of tail, the percentage in DNA tail (TDNA%) and olive tail moment (OTM) induced by SiO2 nanoparticles were significantly increased in comparison with control and microscale SiO2 at 500 mg/mL. 500 mg/mL SiO2 nanoparticles and microscale SiO2 caused a significant increase in apoptosis rate, decreased proliferation index and increased cell proportions in G0/G1 phases by contrast to the negative control (P 2 nanoparticles are more cytotoxic than microscale SiO2 particles; they induce DNA injury, increase apoptosis, and decrease the proliferation index in RAW264.7 cells. DNA injury and apoptosis may be involved in reducing cell proliferation.

Silica (SiO2) nanoparticles are being progressively applied in various applications, including cosmetics, food technology, and medical diagnostics. Although crystalline SiO2 is a known carcinogen, the carcinogenicity of SiO2 nanoparticles remains unclear. Here, we assessed the cytotoxic effects and DNA injury induced by exposure to various dosages of SiO2 nanoparticles at 0-2400 mg/mL (0-3200 mg/mL microscale SiO2 as positive control) for 24 h using RAW264.7 cells, followed by methyl tetrazolium (MTT) assay. Cells were also treated by 31.25, 125, and 500 mg/mL SiO2 nanoparticles (500 mg/mL microscale SiO2 as positive control) for 24 h and examined by single cell gel electrophoresis assay (SCEG) and flow cytometry. Outstanding dose-related decline in cell viability was observed with enhancing dosages of SiO2 nanoparticles by MTT assay. The inhibitory concentration 50% of SiO2 nanoparticles and microscale SiO2 was 16690 and 5080 mg/mL, respectively. The comet rate (comet%), length of tail, the percentage in DNA tail (TDNA%) and olive tail moment (OTM) induced by SiO2 nanoparticles were significantly increased in comparison with control and microscale SiO2 at 500 mg/mL. 500 mg/mL SiO2 nanoparticles and microscale SiO2 caused a significant increase in apoptosis rate, decreased proliferation index and increased cell proportions in G0/G1 phases by contrast to the negative control (P 2 nanoparticles are more cytotoxic than microscale SiO2 particles; they induce DNA injury, increase apoptosis, and decrease the proliferation index in RAW264.7 cells. DNA injury and apoptosis may be involved in reducing cell proliferation.