English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 21921/27947 (78%)
造訪人次 : 4200222      線上人數 : 1022
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://140.128.103.80:8080/handle/310901/24795


    題名: Growth inhibition and antioxidative status induced by selenium-enriched broccoli extract and selenocompounds in DNA mismatch repair-deficient human colon cancer cells
    作者: Tsai, C.-F.;Ou, B.-R.;Liang, Y.-C.;Yeh, J.-Y.
    貢獻者: Department of Animal Science and Biotechnology, Tunghai University
    關鍵詞: Broccoli extract;Cellular glutathione peroxidase (cGPX);Human colon cancer cells;Hydrogen peroxide (H2O2);Selenium
    日期: 2013
    上傳時間: 2014-05-30T02:37:48Z (UTC)
    摘要: The effects of enzymatic-digested Se-enriched broccoli extracts (SeB) and selenocompounds on growth and antioxidative status in human colon cancer cells was investigated in this study. HCT116 and HCT116+Chr.3 cells were treated with selenocompounds (sodium selenite, sodium selenate, Se-Met, MeSeCys) or SeB [high-Se (H-SeB) or low-Se (L-SeB)]. The cytotoxicity induced by selenocompounds in HCT116 cells was not associated with cellular H2O2 level, while the differential cytotoxicity observed by sodium selenite between HCT116 and HCT116+Chr.3 cell lines was related to cellular H2O 2 production with the change in antioxidative enzyme activity, and the restoration of chromosome 3. H-SeB was found to reduce the cellular H 2O2 content in HCT116+Chr.3 cells. The results in this study indicate that regardless of Se content, the cytotoxicity in HCT116 cells of both SeB forms appeared to be H2O2-independent, whereas the cytotoxicity in HCT116+Chr.3 of either SeB form appeared to be H 2O2-dependent with an increase in antioxidative ability for H-SeB. ? 2013 Elsevier Ltd. All rights reserved.
    關聯: Food Chemistry,Vol.139,P.267-273
    顯示於類別:[畜產與生物科技學系所] 期刊論文

    文件中的檔案:

    沒有與此文件相關的檔案.



    在THUIR中所有的資料項目都受到原著作權保護.


    本網站之東海大學機構典藏數位內容,無償提供學術研究與公眾教育等公益性使用,惟仍請適度,合理使用本網站之內容,以尊重著作權人之權益。商業上之利用,則請先取得著作權人之授權。

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