title: Effects of SiO2 nanoparticles on HFL-I activating ROS-mediated apoptosis via p53 pathway.
abstract: Silicon dioxide nanoparticles (SiO(2) NPs) have attracted increasing interest as nanovehicles for delivering drugs, genes and bio-active molecules into cells. However, it is still unknown whether SiO(2) NPs could cause side-effects to normal cells. In the present study, human lung fibroblasts (HFL-Is) were directly exposed to two different sizes of SiO(2) NPs. The effect of size and concentration on cell response was studied by analyzing the cell viability, the ratio of apoptosis and the pathway of cell injury. The results demonstrated that a size-associated and a dose-dependent toxicity of HFL-Is was induced by SiO(2) NPs. Meanwhile, the expression of reactive oxygen species in HFL-I was significantly increased. This activation effect was accompanied by upregulation of p53 expression, release of cytochrome C from chondriosomes, inhibition of Bcl2, and activation of Bax and caspase 9. These findings implied that SiO(2) NPs might induce apoptosis of HFL-Is by stimulating reactive oxygen species release and subsequently causing the activation of p53 pathway in vitro.
authors.affiliation: Shanghai Biomaterials Research and Testing Center, Shanghai, 200023, China.
authors.forename: Zhengli
authors.initials: Z
authors.lastname: Xu
authors.forename: Laisheng
authors.initials: L
authors.lastname: Chou
authors.forename: Jiao
authors.initials: J
authors.lastname: Sun
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D002470:Cell Survival; D005347:Fibroblasts / Q000166:cytology / Q000473:pathology*; D006801:Humans; D053758:Nanoparticles; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012822:Silicon Dioxide / Q000378:metabolism / Q000633:toxicity*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; D012822:Silicon Dioxide