TFEB
亚砷酸钠
mTORC1型
氧化应激
谷胱甘肽
亚砷酸盐
超氧化物歧化酶
丙二醛
DNA损伤
化学
细胞生物学
生物化学
生物
溶酶体
PI3K/AKT/mTOR通路
砷
信号转导
酶
DNA
有机化学
作者
Di Ouyang,Yiren Xiong,Zuqing Hu,Jiayi He,Shanshan He,Renyi Liu,Zenghui Gao,Dalin Hu
出处
期刊:Toxicology
[Elsevier]
日期:2024-05-01
卷期号:504: 153795-153795
标识
DOI:10.1016/j.tox.2024.153795
摘要
The mechanistic target of rapamycin (RAPA) complex 1 (mTORC1) - transcription factor EB (TFEB) pathway plays a crucial role in response to nutritional status, energy and environmental stress for maintaining cellular homeostasis. But there is few reports on its role in the toxic effects of arsenic exposure and the related mechanisms. Here, we show that the exposure of bronchial epithelial cells (BEAS-2B) to sodium arsenite promoted the activation of mTORC1 (p-mTORC1) and the inactivation of TFEB (p-TFEB), the number and activity of lysosomes decreased, the content of reduced glutathione (GSH) and superoxide dismutase (SOD) decreased, the content of malondialdehyde (MDA) increased, the DNA and chromosome damage elevated. Further, when mTORC1 was inhibited with RAPA, p-mTORC1 and p-TFEB down-regulated, GSH and SOD increased, MDA decreased, the DNA and chromosome damage reduced significantly, as compared with the control group. Our data revealed for the first time that mTORC1 - TFEB pathway was involved in sodium arsenite induced lysosomal alteration, oxidative stress and genetic damage in BEAS-2B cells, and it may be a potential intervention target for the toxic effects of arsenic.
科研通智能强力驱动
Strongly Powered by AbleSci AI