ASIA unversity:Item 310904400/7985
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 94286/110023 (86%)
造訪人次 : 21693904      線上人數 : 630
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/310904400/7985


    題名: Mechanism for proliferation inhibition by various selenium compounds and selenium-enriched broccoli extract in rat glial cells
    作者: Yeh, J. Y.;Ou, B. R.;Liang, Y. C.;Burchfiel, J.;Butler, J. A.;Forsberg, N. E.;Whanger, P. D.
    貢獻者: Department of Biotechnology
    關鍵詞: apoptosis;broccoli extract;cellular glutathione peroxidase (cGPX);hydrogen peroxide (H2O2);selenium
    日期: 2006
    上傳時間: 2010-03-15 08:11:07 (UTC+0)
    出版者: Asia University
    摘要: The objective of this study was to investigate the differential effects of various selenium (Se) compounds and Se-enriched broccoli extracts on cell proliferation and the possible mechanism responsible for the Se-induced growth inhibition. C6 rat glial cells were incubated with graded concentrations up to 1000 nM of selenite, selenate, selenomethionine (SeM), Se-methyl-selenocysteine (SeMCys), high-Se broccoli (H-SeB) extract or low-Se broccoli (L-SeB) extract for 24 and 48 h. MTT results indicated that all Se sources and levels examined inhibited C6 cell proliferation at 48 h. The results from cell cycle progression and apoptosis analysis indicated that SeM, SeMCys, H-SeB or L-SeB treatments at the concentration of 1000 nM reduced the cell population in G0/G1 phase, but induced G2/M phase arrest and increased apoptosis and secondary necrosis in C6 cells at 24 h. The populations of apoptotic cells and secondary necrotic cells were increased by all Se sources examined. The COMET assay indicated that there was no significant DNA single-strand break found for all Se treatments in C6 cells for 48 h. In addition, the Se-induced proliferation inhibition may involve a hydrogen peroxide (H2O2)-dependent mechanism with elevated cellular glutathione peroxidase (cGPX) activity. Both H-SeB and L-SeB inhibited C6 cell proliferation but H-SeB was less inhibitory than L-SeB. The proliferation inhibition by H-SeB in C6 cells is apparently related to the increased H2O2 with the elevated cGPX activity, but the inhibition by L-SeB was H2O2-independent without change in cGPX activity.
    關聯: BioMetals 19(6):611-621
    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
    0KbUnknown473檢視/開啟
    310904400-7985.doc38KbMicrosoft Word152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