Oxidative stress of silica nanoparticles in human bronchial epithelial cell, Beas-2B.

In this study, the potentially harmful effect of the exposure to fumed and porous silicon dioxide (silica) nanoparticles was investigated using human bronchial epithelial cell, Beas-2B, with a focus on the involvement of oxidative stress as the toxic mechanism. Silica nanoparticles-induced oxidative stress was assessed by examining the formation of reactive oxygen species (ROS) and induction of antioxidant enzymes, such as superoxide dismutase (SOD) and heme oxygenase-1 (HO-1). Subsequently, to understand the mechanism of nanoparticles-induced oxidative stress, the involvement of oxidative stress-responding transcription factors, such as, nuclear factor-kappaB (NF-kappaB) and nuclear factor-E2-related factor-2 (Nrf-2), as well as the mitogen-activated protein (MAP) kinase signal transduction pathway were investigated. From the overall results, silica nanoparticles exerted toxicity via oxidative stress, which lead to the induction of HO-1 via the Nrf-2-ERK MAP kinase signaling pathway; cells exposed to porous silica nanoparticles showed a more sensitive response than those exposed to fumed silica. Nevertheless, the parameters tested were rather limited in terms of gaining a full understanding of the oxidative stress and cellular response due to exposure to silica nanoparticles. Further studies on the mechanism by which silica nanoparticles induce the Nrf-2-ERK MAP kinase pathway, to more clearly elucidate the silica-induced oxidative stress, as well as on the relationship between the physico-chemical properties of nanoparticles and their cytotoxicity are warranted to gain an understanding of the phenomenon of different sensitivities between porous and fumed silica.