4.6 Article

Unveiling the Antibacterial Mechanism of Gold Nanoclusters via In Situ Transmission Electron Microscopy

期刊

ACS SUSTAINABLE CHEMISTRY & ENGINEERING
卷 10, 期 1, 页码 464-471

出版社

AMER CHEMICAL SOC
DOI: 10.1021/acssuschemeng.1c06714

关键词

nanocluster; in situ TEM; antibacterial mechanism; real-time observation; reactive oxygen species

资金

  1. Ministry of Science and Technology, Taiwan [MOST 109-2113-M-038-005-MY2]
  2. Taipei Medical University

向作者/读者索取更多资源

Metal nanoclusters have unique properties that make them emerging nanoantibiotics for fighting bacterial infections. Gold nanoclusters, when applied as antibacterial agents, have been shown to destroy bacterial membranes by inducing intracellular reactive oxygen species generation, ultimately leading to bacterial death.
Metal nanoclusters (NCs) with unique chemical and physical properties have been extensively demonstrated to be emerging nanoantibiotics for fighting bacterial infections. Under-standing the antibacterial mechanisms of metal nanoclusters is important for evaluating their clinical applications as nanoantibiotics. To understand the antibacterial mechanism, gold nanoclusters (AuNCs) were applied as an antibacterial agent for real-time observations of their interactions with bacteria by in situ transmission electron microscopy (TEM). In this work, a surface ligand of glutathione-conjugated (GSH)-AuNCs was prepared via a simple hydrothermal method. Optical and structural characterizations validated the successful preparation of GSH-AuNCs. Bacterial growth curves of Acetobacter aceti revealed that the antibacterial activity of GSH-AuNCs increased with the weight concentration. The antibacterial activity of GSH-AuNCs was confirmed by the intracellular reactive oxygen species (ROS) generation induced by GSH-AuNCs in A. aceti. Furthermore, real-time observations of interactions between GSH-AuNCs and A. aceti were made using in situ liquid cell TEM. Based on the results of realtime observations, GSH-AuNCs first attached onto the bacterial membranes of A. aceti by physical adsorption and then penetrated into A. aceti by internalization. Eventually, the production of intracellular ROS induced by GSH-AuNCs caused destruction of the bacterial membranes, which led to the death of A. aceti. After the bacterial membranes had been destroyed, A. aceti eventually died.

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