自噬
粒体自噬
活性氧
溶酶体
细胞生物学
线粒体
细胞毒性
化学
乙酰半胱氨酸
线粒体ROS
脐静脉
程序性细胞死亡
细胞凋亡
细胞损伤
生物
生物化学
体外
抗氧化剂
酶
作者
Jian‐Qing He,Yue Ma,Xinli Niu,Junchen Pei,Rong Yan,Fangjing Xu,Jun Ma,Xiaobo Ma,Shanshan Jia,Wenjian Ma
出处
期刊:Toxicology
[Elsevier]
日期:2024-02-01
卷期号:502: 153734-153734
被引量:1
标识
DOI:10.1016/j.tox.2024.153734
摘要
Silver nanoparticles (AgNPs) are used increasingly often in the biomedical field, but their potential deleterious effects on the cardiovascular system remain to be elucidated. The primary aim of this study was to evaluate the toxic effects, and the underlying mechanisms of these effects, of AgNPs on human umbilical vein endothelial cells (HUVECs), as well as the protective role of N-acetylcysteine (NAC) against cytotoxicity induced by AgNPs. In this study, we found that exposure to AgNPs affects the morphology and function of endothelial cells which manifests as decreased cell proliferation, migration, and angiogenesis ability. Mechanistically, AgNPs can induce excessive cellular production of reactive oxygen species (ROS), leading to damage to cellular sub-organs such as mitochondria and lysosomes. More importantly, our data suggest that AgNPs causes autophagy defect, inhibits mitophagy, and finally activates the mitochondria-mediated apoptosis signaling pathway and evokes cell death. Interestingly, treatment with ROS scavenger-NAC can effectively suppress AgNP-induced endothelial damage.Our results indicate that ROS-mediated mitochondria-lysosome injury and autophagy dysfunction are potential factors of endothelial toxicity induced by AgNPs. This study may provide new evidence for the cardiovascular toxicity of AgNPs and serve as a reference for the safe use of nanoparticles(NPs) in the future.
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