ASIA unversity:Item 310904400/7979
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 94286/110023 (86%)
造訪人次 : 21660262      線上人數 : 511
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧:
  • 您可在西文檢索詞彙前後加上"雙引號",以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋,建議至進階搜尋限定作者欄位,可獲得較完整資料
  • 進階搜尋


    請使用永久網址來引用或連結此文件: http://asiair.asia.edu.tw/ir/handle/310904400/7979


    題名: Differential influences of various arsenic compounds on glutathione redox status and antioxidative enzymes in porcine endothelial cells.
    作者: Yeh, J. Y.;Cheng, L. C.;Ou, B. R.;Whanger, P. D.;Chang, L. W.
    貢獻者: Department of Biotechnology
    關鍵詞: Biochemistry & Molecular Biology;Cell Biology
    日期: 2002
    上傳時間: 2010-03-15 08:11:02 (UTC+0)
    出版者: Asia University
    摘要: The cellular response and detoxification mechanisms in porcine endothelial cells (PAECs) to arsenic trioxide (As2O3), sodium arsenite (NaAsO2) and sodium arsenate (Na2HAsO4,) were investigated. NaAsO2 at 20 muM for 72 h increased Cu/Zn superoxide dismutase activity resulting in elevated intracellular hydrogen peroxide levels, but As2O3 and Na2HAsO4 did not. Trivalent arsenic compounds increased intracellular oxidized glutathione (GSSG) and total glutathione (GSH) and cellular glutathione peroxidase (cGPX) and glutathione S-transferase (GST) activity, but not glutathione reductase activity. The increased cGPX activity resulted in an elevated cellular GSSG content. Na2HAsO4 increased the cellular GSSG level at 72 h compared to controls. These results imply that the increased GSH content responding to the oxidative stress by trivalent arsenic compounds may be mainly related to the regulation of GSH turnover. The increased GST activity implies that the elevated intracellular GSH level responding to the oxidative stress may be used to conjugate arsenic in PAECs and facilitate arsenic efflux.
    關聯: Cellular and Molecular Life Sciences 59:1972-1982
    顯示於類別:[生物科技學系] 期刊論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    0KbUnknown375檢視/開啟
    310904400-7979 .doc31KbMicrosoft Word191檢視/開啟


    在ASIAIR中所有的資料項目都受到原著作權保護.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回饋