Department of Toxicology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR China.
Toxicol In Vitro. 2011 Dec;25(8):1619-29. doi: 10.1016/j.tiv.2011.06.012. Epub 2011 Jun 24.
Amorphous silica nanoparticles are widely applied in many fields. But the adverse effects of silica nanoparticle exposure were unclear. The present study investigated the cytotoxicity and mitochondrial damage of silica nanoparticles exposure in hepatocellular carcinoma cell line (HepG2). The cells were treated with 43 nm non-modified amorphous silica nanoparticles which dispersed in serum-free DMEM at concentrations of 0, 25, 50, 100 and 200 μg/mL for 3 and 24 h. The results showed that the silica nanoparticles could lead to increasing cellular reactive oxygen species (ROS) production for 3 and 24 h exposure. Moreover, the oxidative stress induced by the particles could play an important role of the mitochondrial membrane damage and the cell apoptosis. It indicated that apoptosis through mitochondrial pathway mediated by oxidative stress was a potential mechanism of cytotoxicity induced by silica nanoparticles. The particles could enter the cells through different pathways and dispersed in cytoplasm and deposited inside mitochondria. Mitochondria were the major organelles for the cytotoxicity of silica nanoparticles exposure. Mitochondrial damage was related to the oxidative stress and the direct injurious effect of nanoparticles. It can be considered as the potential mechanism for the cytotoxic effects of amorphous silica nanoparticles.
无定形二氧化硅纳米颗粒被广泛应用于许多领域。然而，二氧化硅纳米颗粒暴露的不良影响尚不清楚。本研究探讨了暴露于无定形二氧化硅纳米颗粒（粒径为 43nm，未经修饰，分散于无血清 DMEM 中）对肝癌细胞系（HepG2）的细胞毒性和线粒体损伤的影响。细胞分别用浓度为 0、25、50、100 和 200μg/mL 的纳米颗粒处理 3 和 24 h。结果表明，纳米颗粒暴露 3 和 24 h 后可导致细胞内活性氧（ROS）产生增加。此外，颗粒诱导的氧化应激可能在线粒体膜损伤和细胞凋亡中起重要作用。这表明通过氧化应激介导的线粒体途径的细胞凋亡是二氧化硅纳米颗粒诱导细胞毒性的潜在机制。颗粒可通过不同途径进入细胞，分散在细胞质中，并沉积在内线粒体中。线粒体是二氧化硅纳米颗粒暴露引起细胞毒性的主要细胞器。线粒体损伤与氧化应激和纳米颗粒的直接损伤作用有关。这可以被认为是无定形二氧化硅纳米颗粒细胞毒性作用的潜在机制。
