SiO(2) Nanoparticles Induced Cytotoxicity by Oxidative Stress in Human Bronchial Epithelial Cell, Beas-2B

In this study, we investigated the potential harmful effect of the exposure to silicon dioxide (SiO(2)) nanoparticles through in vitro toxicity assay using human bronchial epithelial cell, Beas-2B with a focus on the involvement of oxidative stress as the toxic mechanism.

SiO(2)-induced oxidative stress was assessed by examining formation of reactive oxygen species (ROS), the induction of superoxide dismutase (SOD) and heme oxygenase-1 (HO-1), as well as cytotoxicity effect was evaluation by cell viability. Subsequently, to understand the molecular mechanism of nanoparticle-induced oxidative stress, the involvement of oxidative stress-responding transcription factors, such as, nuclear factor-kappaB (NF-κB) and nuclear factor-E2-related factor-2 (Nrf-2), and mitogen-activated protein (MAP) kinase signal transduction pathway was also investigated.

5-d i phenyltera zolium bromide (MTT) assay results show that decrease 20% in cell viability and the number of cells in the subG1 phase increased. The increase in ROS formation was observed in SiO(2) nanoparticle treated cells. The expression of SOD protein was not changed, whereas that of HO-1 was increased by SiO(2) nanoparticle exposure. transcription factors Nrf-2 and the expression of phosphorylated form of extracellular signal-regulating kinase (ERK) was strongly induced by SiO(2) nanoparticle exposure

SiO(2) nanoparticles exert their toxicity through oxidative stress as they cause the significant increase ROS level. SiO(2) nanoparticles induce induction of HO-1 via Nrf-2-ERK MAP kinase pathway. Our tested oxidative stress parameters are rather limited in terms of allowing the full understanding of oxidative stress and cellular response by SiO(2) nanoparticle exposure.