中山醫學大學機構典藏 CSMUIR:Item 310902500/18550
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    题名: nduction of Oxidative Stress and DNA Damage in Human Renal Proximal Tubular Cells by Aristolochic Acid
    作者: Yu, FENG-YIH
    Chu, Ting-Yen
    Lian, Jong-Da
    Wu, Sheng-Wen
    Hung, Tung-Wei
    Chang, Horng-Rong
    贡献者: 中山醫大
    关键词: aristolochic acid;reactive oxygen species;DNA damage;馬兜鈴酸;活性氧分子;DNA傷害
    馬兜鈴酸;活性氧分子;DNA傷害
    日期: 2011-07-04
    上传时间: 2017-11-13T03:37:45Z (UTC)
    出版者: Journal of Food and Drug Analysis
    摘要: ABSTRACT

    Aristolochic acid I (AAI) is found primarily in the plant Aristolochia. Consumption of products containing AAI has been linked with permanent kidney damage and urothelial carcinoma. This study applied human proximal tubule epithelial cell line (HK-2) to examine the relationship among AAI-induced intracellular oxidative stress, DNA damage and MAP kinase activation. High concentrations of AAI caused a decrease in cell viability and an increase in the activity of caspase 3. AAI treatment also led to a dose-dependent increase of reactive oxygen species (ROS) in HK-2 cells, and the presence of antioxidant glutathione (GSH) effectively inhibited ROS generation. Stimulating HK-2 cultures with AAI also led to GSH depletion. Results from single cell gel electrophoresis (SCGE) assays demonstrated that AAI showed the ability to increase the levels of DNA strand breaks in HK-2 cells. Up-regulation of luciferase activity driven by the Nrf2 binding element was also observed after 200 µM AAI treatment. Exposure of HK-2 cells with AAI activated both ERK1/2 and p38 kinase phosphorylation, while only the MEK1/2 inhibitor, U0126, significantly decreased the levels of AAI-mediated ROS. In addition, both U0126 and SB202190 effectively reversed the levels of DNA damage triggered by AAI. This suggests that AAI treatment of HK-2 results in ROS formation and DNA damage. Furthermore, ROS generation occurs via the MEK/ERK1/2 signaling pathway, whereas DNA damage occurs via both the ERK1/2 and p38 pathways.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/18550
    關聯: Journal of Food and Drug Analysis 19:2 2011.06[民100.06] 頁114-122+239
    显示于类别:[醫學研究所] 期刊論文

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