English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 29490/55136 (53%)
造訪人次 : 1498568      線上人數 : 110
RC Version 7.0 © 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
    主頁登入上傳說明關於CMUR管理 到手機版
    請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/30076


    題名: Inhibitory actions of glycyrrhizic acid on arylamine N-acetyltransferase activity in strains of Helicobacter pylori from peptic ulcer patients
    作者: Chung, JG
    貢獻者: 醫學院醫學系;China Med Coll, Dept Med, Taichung 400, Taiwan
    日期: 1998
    上傳時間: 2010-09-24 14:48:46 (UTC+8)
    出版者: MARCEL DEKKER INC
    摘要: Arylamine N-acetyltransferase (NAT) activity in Helicobacter pylori was inhibited by ellagic acid, a possible chemopreventive drug. The NAT activity was determined using an acetyl CoA recycling assay and high pressure liquid chromatography. Inhibition of growth studies using H. pylori demonstrated that ellagic acid elicited a dose-dependent bactericidal effect in H. pylori cultures, i.e. the greater the concentration of ellagic acid, the greater the inhibition of growth of H. pylori. The IC50 value was 1 mM for inhibition of growth of H. pylori. Cytosols or suspensions of H. pylori with and without selected concentrations of ellagic acid co-treatment showed different percentages of 2-aminofluorene and p-aminobenzoic acid acetylation. The data indicated that there was decreased NAT activity associated with increased ellagic acid in H. pylori cytosols and intact cells. For the cytosol and intact bacteria examinations, the apparent values of K-m and V-max decreased after co-treatment with 1 mM ellagic acid. This report is the first demonstration of ellagic acid inhibition of arylamine NAT activity and ellagic acid inhibition of growth in the bacterium H. pylori.
    關聯: DRUG AND CHEMICAL TOXICOLOGY 21(3):355-370
    顯示於類別:[醫學系] 期刊論文

    文件中的檔案:

    沒有與此文件相關的檔案.



    在CMUR中所有的資料項目都受到原著作權保護.

    TAIR相關文章

     


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