Biomaterials生物材料Biomaterials生物材料.doc

Biomaterials生物材料 Influence of particle size and reactive oxygen species on cobalt chrome nanoparticle-mediated genotoxicity粒子大小和活性氧对钴铬nanoparticle-mediated基因毒性 nanoparticle-mediatedPatients with cobalt chrome (CoCr) metal-on-metal (MOM) implants may be exposed to a wide size range of metallic nanoparticles as a result of wear. 患者钴铬(CoCr)金属对金属介面人工髋关节(MOM)植入可能接触到广泛的大小金属纳米粒子由于穿的范围。In this study we have characterised the biological responses of human fibroblasts to two types of synthetically derived CoCr particles [(a) from a tribometer (30 nm) and (b) thermal plasma technology (20, 35, and 80 nm)] in vitro, testing their dependence on nanoparticle size or the generation of oxygen free radicals, or both. 在这项研究中我们有特征的生物综合反应人类成纤维细胞的两种类型的派生CoCr粒子(从摩擦计(a) (30 nm)和(b)热等离子体技术(20,35岁,和80海里)体外,测试的依赖纳米粒子大小或氧自由基的生成,或两者兼而有之。 Metal ions were released from thesurface of nanoparticles, particularly from larger (80 nm) particles generated by thermal plasma technology. 金属离子被释放纳米颗粒的表面,特别是从大(80海里)粒子产生的热等离子体技术。 Exposure of fibroblasts to these nanoparticles triggered rapid (2 h) generation of reactive oxygen species (ROS) that could be eliminated by inhibition of NADPH oxidase, suggesting that it was mediated by phagocytosis of the particles. 成纤维细胞接触到这些纳米粒子快速触发(2 h)代的活性氧物种(ROS),可以消除NADPH氧化酶的抑制作用,表明这是介导吞噬作用的粒子。 The exposure also caused a more prolonged, MitoQ sensitive production of ROS (24 h), suggesting involvement of mitochondria曝光也引起了更长期,MitoQ敏感的生产ROS(24小时),这表明线粒体的参与 Consequently, we recorded elevated levels of aneuploidy, chromosome clumping, fragmentation of mitochondria and damage to the cytoskeleton particularly to the microtubule network. 因此,我们记录的水平升高非整倍性染色体聚集,线粒体的分裂和破坏细胞骨架尤其是微管网络。 Exposure to the nanoparticles resulted in misshapen nuclei, disruption of mature lamin B1 and increased nucleoplasmic bridges, which could be prevented by MitoQ. 暴露于纳米颗粒导致畸形细胞核,中断成熟的核纤层蛋白B1和核质增加桥梁、MitoQ可以预防的。 In addition, increased numbers of micronuclei were observed and these were only partly prevente