DNA damage response to different surface chemistry of silver nanoparticles in mammalian cells

DNA damage response to different surface chemistry of silver nanoparticles in mammalian cells
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DOI:
10.1016/j.taap.2008.09.015
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发表时间:
2008-12-15
影响因子:
3.8
通讯作者:
Hong, Yiling
Hong, Yiling
中科院分区:
医学3区
文献类型:
--
作者:
Ahamed, Maqusood;Karns, Michael;Hong, Yiling

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被引文献

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最近,银纳米颗粒(Ag NPs)因其在生物技术和生命科学中的可能应用而受到广泛关注。银纳米颗粒对于国防和工程计划的新材料应用以及作为抗微生物剂的商业目的是有意义的。然而,很少有人知道的遗传毒性的银纳米颗粒暴露于哺乳动物细胞。本研究旨在研究两种类型的哺乳动物细胞(小鼠胚胎干细胞(mES)和小鼠胚胎成纤维细胞(MEF))中多糖表面功能化(涂覆)和非功能化(未涂覆)Au纳米粒子的DNA损伤反应。这两种类型的银纳米颗粒上调细胞周期检查点蛋白p53和DNA损伤修复蛋白Rad51和磷酸化H2AX的表达。此外,通过膜联蛋白V蛋白表达和MTT测定,它们均诱导细胞死亡。我们的观察结果还表明,不同的表面化学的银纳米粒子诱导不同的DNA损伤反应:涂覆的银纳米粒子表现出更严重的损伤比未涂覆的银纳米粒子。结果表明,多糖包衣颗粒更独立地分布,而未包衣颗粒的团聚限制了表面积的可用性和对膜结合细胞器的访问。爱思唯尔公司出版
Silver nanoparticles (Ag NPs) have recently received much attention for their possible applications in biotechnology and life sciences. Ag NPs are of interest to defense and engineering programs for new material applications as well as for commercial purposes as an antimicrobial. However, little is known about the genotoxicity of Ag NPs following exposure to mammalian cells. This study was undertaken to examine the DNA damage response to polysaccharide surface functionalized (coated) and non-functionalized (uncoated) Au NPs in two types of mammalian cells; mouse embryonic stein (mES) cells and mouse embryonic fibroblasts (MEF). Both types of Ag NPs up-regulated the cell cycle checkpoint protein p53 and DNA damage repair proteins Rad51 and phosphorylated-H2AX expression. Furthermore both of them induced cell death as measured by the annexin V protein expression and MTT assay. Our observations also suggested that the different surface chemistry of Ag NPs induce different DNA damage response: coated Ag NPs exhibited more severe damage than uncoated Ag NPs. The results suggest that polysaccharide coated particles are more individually distributed while agglomeration of the uncoated particles limits the surface area availability and access to membrane bound organelles. Published by Elsevier Inc.