Issue 11, 2020

Initiation of protective autophagy in hepatocytes by gold nanorod core/silver shell nanostructures

Abstract

The high reactivity of silver nanoparticles leads to their broad applications in the anti-bacterial field; however, the safety of silver nanoparticles has attracted increasing public attention. After exposure to silver nanoparticles in vivo, the liver serves as their potential deposition site; however the potential biological effects of such nanoparticles on hepatocytes at low dosages are not well understood. Here, we study the interaction between gold nanorod core/silver shell nanostructures (Au@Ag NRs) and human hepatocytes, HepG2 cells, and determine that Au@Ag NRs at sub-lethal doses can induce autophagy. After uptake, Au@Ag NRs mainly localize in the lysosomes where they release silver ions and promote the production of reactive oxygen species (ROS). The ROS then suppress the AKT-mTOR signaling pathway and activate autophagy. In addition, oxidative stress results in lysosomal impairment, causing decreased ability for lysosomal digestion. Moreover, oxidative stress also affects the structure and function of mitochondria, leading to the initiation of protective autophagy to eliminate the damaged mitochondrion. Our study shows that at sub-lethal dosages, silver nanomaterials may alter the physiological functions of hepatic cells by activating protective autophagy and cause potential health risks, indicating that cautious consideration of the safety of nanomaterials for certain applications is necessary.

Graphical abstract: Initiation of protective autophagy in hepatocytes by gold nanorod core/silver shell nanostructures

Supplementary files

Article information

Article type
Paper
Submitted
08 okt 2019
Accepted
11 fev 2020
First published
11 fev 2020

Nanoscale, 2020,12, 6429-6437

Initiation of protective autophagy in hepatocytes by gold nanorod core/silver shell nanostructures

H. Li, J. Chen, H. Fan, R. Cai, X. Gao, D. Meng, Y. Ji, C. Chen, L. Wang and X. Wu, Nanoscale, 2020, 12, 6429 DOI: 10.1039/C9NR08621H

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