中大機構典藏-NCU Institutional Repository-提供博碩士論文、考古題、期刊論文、研究計畫等下載:Item 987654321/50854
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 80990/80990 (100%)
Visitors : 41947818      Online Users : 1376
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version


    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/50854


    Title: The down-regulation of galectin-1 expression is a specific biomarker of arsenic toxicity
    Authors: Chang,YY;Chiang,MC;Kuo,TC;Chi,LL;Kao,YH;Huang,RN
    Contributors: 生命科學系
    Keywords: ACUTE PROMYELOCYTIC LEUKEMIA;HAMSTER OVARY CELLS;ACTIVATED RAT MACROPHAGES;RNA INTERFERENCE;DRINKING-WATER;TRIOXIDE AS2O3;LYMPHOBLASTOID-CELLS;FUNCTIONAL-ANATOMY;CLINICAL-EFFICACY;BINDING-PROTEINS
    Date: 2011
    Issue Date: 2012-03-27 18:11:28 (UTC+8)
    Publisher: 國立中央大學
    Abstract: Galectin-1 (GAL1) is known as a beta-galactoside-binding protein that also can bind with arsenic to regulate cell functions. Using RNA interference technique, we investigated the possible mechanism. involved in GAL1 modulation of arsenite-inhibited cell survival in 3T3 fibroblast and KB oral cancer cells. GAL1 gene knockdown significantly attenuated sodium arsenite (NaAsO(2)) and arsenic trioxide (As(2)O(3)) inhibition of cell survival. However, GAL1 gene knockdown did not alter the inhibition of cell survival by antimony chloride, cadmium chloride or nickel sulfate. These results suggested the GAL1 selectively affects particular types of heavy metal elements. Flow cytometric analysis indicated GAL1 gene knockdown also suppressed As(III)-stimulated levels of sub-G1 and G2/M growth arrest in both cells. Moreover, atomic absorption spectrophotometric results showed that GAL1 gene knockdown reduced the total arsenic accumulation of both cells after the NaAsO(2) and As(2)O(3) treatment. These results suggested that GAL1 gene knockdown mediates the apoptotic effects of arsenic in 3T3 and KB cells via regulation of the cellular arsenic levels. We propose that down-regulation of GAL1 expression may be a useful and specific biomarker in assessing the toxicity of arsenic exposure. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
    Relation: TOXICOLOGY LETTERS
    Appears in Collections:[Department of Life Science] journal & Dissertation

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML581View/Open


    All items in NCUIR are protected by copyright, with all rights reserved.

    社群 sharing

    ::: Copyright National Central University. | 國立中央大學圖書館版權所有 | 收藏本站 | 設為首頁 | 最佳瀏覽畫面: 1024*768 | 建站日期:8-24-2009 :::
    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 隱私權政策聲明