Nanosilver Targets the Bacterial Cell Envelope: The Link with Generation of Reactive Oxygen Radicals

Nanosilver Targets the Bacterial Cell Envelope: The Link with Generation of Reactive Oxygen Radicals
复制标题

DOI:
10.1021/acsami.9b20193
复制
发表时间:
2020-02-05
影响因子:
9.5
通讯作者:
Amal, Rose
Amal, Rose
中科院分区:
材料科学2区
文献类型:
--
作者:
Gunawan, Cindy;Faiz, Merisa B.;Amal, Rose

文献摘要

被引文献

相似文献

这项工作描述了纳米银(NAg)与细菌细胞包膜成分在分子水平上的相互作用,以及这如何与活性氧(ROS)介导的纳米颗粒毒性相关。在细胞包膜生物分子中检测到主要的结构变化,作为功能部分,如氨基,酰胺和磷酸二酯的损伤的结果。NAg暴露使主要细胞壁组分肽聚糖中的聚糖骨架解体,导致脂磷壁酸完全分解,并破坏磷脂酰乙醇胺(一种膜磷脂)中的磷酸-胺和脂肪酸基团。与氧化攻击一致,我们提出,所观察到的细胞被膜损伤至少部分是由纳米颗粒在其浸出过程中产生的活性氧自由基造成的,非生物地,没有细胞。细胞包膜靶向,特别是内膜磷脂上的那些,可能随后触发致死水平的细胞超氧化物(O-2(中心点-))和羟基(OH中心点)自由基的快速产生,在本文中用模型细菌观察到。本研究提供了对NAg的抗菌机制的更好理解,其中ROS的产生可能是毒性的原因和后果,与纳米颗粒靶向的初始细胞包膜相关。
The work describes the interactions of nanosilver (NAg) with bacterial cell envelope components at a molecular level and how this associates with the reactive oxygen species (ROS)-mediated toxicity of the nanoparticle. Major structural changes were detected in cell envelope biomolecules as a result of damages in functional moieties, such as the saccharides, amides, and phosphodiesters. NAg exposure disintegrates the glycan backbone in the major cell wall component peptidoglycan, causes complete breakdown of lipoteichoic acid, and disrupts the phosphate-amine and fatty acid groups in phosphatidylethanolamine, a membrane phospholipid. Consistent with the oxidative attacks, we propose that the observed cell envelope damages are inflicted, at least in part, by the reactive oxygen radicals being generated by the nanoparticle during its leaching process, abiotically, without cells. The cell envelope targeting, especially those on the inner membrane phospholipid, is likely to then trigger the rapid generation of lethal levels of cellular superoxide (O-2(center dot-)) and hydroxyl (OH center dot) radicals herein seen with a model bacterium. The present study provides a better understanding of the antibacterial mechanisms of NAg, whereby ROS generation could be both the cause and consequence of the toxicity, associated with the initial cell envelope targeting by the nanoparticle.