Study On Cytotoxicity Of Silica Nanoparticles On Human Lung Cancer Cells

Silica (SiO2) nanoparticles have shown great promise for use as tools in a wide variety of biomedical applications. The environmental and health impact of nanomaterials is of great interest. This study was undertaken to evaluate potential toxicity and the general mechanism involved in nanoparticle toxicity, the provide available guidelines to quantify their effects.The study evaluated the acute toxic effects of SiO2nanoparticles (nano-SiO2) using human lung alveolar carcinoma epithelial (A549) cells. Different sizes of SiO2nanoparticles (25and50nm) wer.e evaluated for their potential toxicity. For toxicity evaluations, cellular morphology, cell viability (MTT assay), reactive oxygen species (ROS), nitric oxide (NO), hydrogen peroxide (H2O2), radical anion (O2-), Hydroxyl Radical (OH), malonaldehyde (MDA), cell membrane decrease of ATPase, cell apoptosis and necrosis were assessed under control and silica exposed conditions.The results on A549cells showed that exposure to increasing concentrations of nano-SiO2, from20to150μg/ml, resulted in a dose-dependent diminishing viability of A549cells. Median lethal dose (LD50) of20-and50-nm SiO2nanoparticles showed30±3.73μg/ml,120±13.82μg/ml in24h, respectively. Morphological examination revealed cell shrinkage along with large numbers of apoptosis bodies. Increase in intracellular ROS, NO, H2O2, O2-，OH*and MDA production and decrease of ATPase content were also observed、in nano-SiO2-exposed A549cells, suggested an elevated level of oxidative stress and lipid peroxidation, the decrease of ATPase indicated that nano-SiO2induced cellular membrane damage. The fluorescence microscope revealed the dose-dependent apoptosis and necrosis in nano-Si02-exposed A549cells.For the mechanism of nano-SiO2-induced cytotoxicity, we found that excessive ROS generation and oxidative stress contributed to nano-SiO2-induced cytotoxicity in A549cells. Nano-SiO2was taken up by cells, and caused excessive ROS and MDA generation, cell membrane decrease of ATPase, mitochondria and cell dysfunction, cell proliferation inhibition and induce cell apoptosis and necrosis.