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PIN1-mediated ROS production is involved in antagonism of N-acetyl-L-cysteine against arsenic-induced hepatotoxicity.

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第一作者： Huijie,Zhang

第一单位： Medical College, Guangxi University, 100 University East Road, Xixiangtang District, Nanning, Guangxi, 530004, P. R. China.

作者： Huijie,Zhang ^[1] ; Zhixin,He ^[2] ; Ping,Deng ^[2] ; Muxue,Lu ^[1] ; Chao,Zhou ^[2] ; Lingling,Yang ^[2] ; Zhengping,Yu ^[1]

作者单位： Medical College, Guangxi University, 100 University East Road, Xixiangtang District, Nanning, Guangxi, 530004, P. R. China. ^[1] Department of Occupational Health, Third Military Medical University, 30 Gaotanyan Zhengjie, Shapingba District, Chongqing, 400038, P. R. China. ^[2]

关键词 PIN1 ROS arsenic hepatotoxicity mitochondrial dysfunction

DOI 10.1093/toxres/tfac040

PMID 36051664

发布时间 2023-07-09

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Toxicology research

2022年11卷4期

628-643页

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Toxicology research

2022年11卷4期

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PIN1-mediated ROS production is involved in antagonism of N-acetyl-L-cysteine against arsenic-induced hepatotoxicity.

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PIN1-mediated ROS production is involved in antagonism of N-acetyl-L-cysteine against arsenic-induced hepatotoxicity.

Toxicology research

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