Anti-proliferative activity of silver nanoparticles.
Anti-proliferative activity of silver nanoparticles.
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DOI：
10.1186/1471-2121-10-65
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发表时间：
2009-09-17
期刊：
影响因子：
--
通讯作者：
Valiyaveettil S
中科院分区：
文献类型：
--
作者：
Asharani PV;Hande MP;Valiyaveettil S
纳米颗粒具有特殊的物理和化学性质，导致快速商业化。银纳米颗粒（Ag-np）由于其抗微生物潜力而属于最商业化的纳米颗粒。银纳米粒子在化妆品、治疗剂和家用产品中的广泛应用，引起了公众对它们与人类和环境使用相关的安全性的关注。实际上没有关于使用这些纳米材料的安全法规。纳米材料与细胞的相互作用、吸收机制、分布、排泄、毒理学终点和作用机制仍然没有答案。将不同剂量的Ag-nps作用于正常人肺成纤维细胞（IMR-90）和人胶质母细胞瘤细胞（U251）。Ag-nps的摄取主要通过内吞作用（网格蛋白介导的过程和巨胞饮作用）发生，同时伴随着时间依赖性的胞吐速率增加。电镜下Ag-np在细胞质和细胞核中呈均匀分布。银纳米粒子处理的细胞表现出染色体不稳定性和有丝分裂阻滞在人类细胞。正常人成纤维细胞从停滞中有效恢复，而癌细胞停止增殖。Ag-np的毒性是通过细胞内钙（Ca 2+）瞬变沿着细胞形态和扩散以及表面褶皱的显著改变来介导的。Ag-NP暴露后，观察到主要肌动蛋白结合蛋白细丝蛋白的下调。银核蛋白诱导的胁迫导致金属硫蛋白和血红素加氧酶-1基因表达上调。在这里，我们表明，摄取银核蛋白主要是通过网格蛋白介导的内吞作用和巨胞饮作用。我们的研究结果表明，癌细胞容易受到损害，缺乏从银-NP诱导的压力恢复。银核蛋白被发现是通过细胞内钙瞬变和染色体畸变，直接或通过激活分解代谢酶。信号级联被认为在细胞骨架变形中起关键作用，并最终抑制细胞增殖。
Nanoparticles possess exceptional physical and chemical properties which led to rapid commercialisation. Silver nanoparticles (Ag-np) are among the most commercialised nanoparticles due to their antimicrobial potential. Ag-np based cosmetics, therapeutic agents and household products are in wide use, which raised a public concern regarding their safety associated with human and environmental use. No safety regulations are in practice for the use of these nanomaterials. The interactions of nanomaterials with cells, uptake mechanisms, distribution, excretion, toxicological endpoints and mechanism of action remain unanswered. Normal human lung fibroblasts (IMR-90) and human glioblastoma cells (U251) were exposed to different doses of Ag-nps in vitro. Uptake of Ag-nps occurred mainly through endocytosis (clathrin mediated process and macropinocytosis), accompanied by a time dependent increase in exocytosis rate. The electron micrographs revealed a uniform intracellular distribution of Ag-np both in cytoplasm and nucleus. Ag-np treated cells exhibited chromosome instability and mitotic arrest in human cells. There was efficient recovery from arrest in normal human fibroblasts whereas the cancer cells ceased to proliferate. Toxicity of Ag-np is mediated through intracellular calcium (Ca2+) transients along with significant alterations in cell morphology and spreading and surface ruffling. Down regulation of major actin binding protein, filamin was observed after Ag-np exposure. Ag-np induced stress resulted in the up regulation of metallothionein and heme oxygenase -1 genes. Here, we demonstrate that uptake of Ag-np occurs mainly through clathrin mediated endocytosis and macropinocytosis. Our results suggest that cancer cells are susceptible to damage with lack of recovery from Ag-np-induced stress. Ag-np is found to be acting through intracellular calcium transients and chromosomal aberrations, either directly or through activation of catabolic enzymes. The signalling cascades are believed to play key roles in cytoskeleton deformations and ultimately to inhibit cell proliferation.
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DOI：
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