國家衛生研究院 NHRI:Item 3990099045/2454
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 857810      Online Users : 831
RC Version 6.0 © 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
    Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer Goto mobile version


    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/2454


    Title: 4-Methoxyestradiol-induced oxidative injuries in human lung epithelial cells
    Authors: Cheng, Y;Chang, LW;Cheng, LC;Tsai, MH;Lin, PP
    Contributors: Division of Environmental Health and Occupational Medicine
    Abstract: Epidemiological studies indicated that people exposed to dioxins were prone to the development of lung diseases including lung cancer. Animal studies demonstrated that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased liver tumors and promoted lung metaplasia in females. Metabolic changes in 17 beta-estradiol (E-2) resulted from an interaction between TCDD and E-2 could be associated with gender difference. Previously, we reported that methoxylestradiols (MeOE2), especially 4-MeOE2, accumulated in human lung cells (BEAS-2B) co-treated with TCDD and E-2. In the present study, we demonstrate unique accumulation of 4-MeOE2, as a result of TCDD/E-2 interaction and revealed its bioactivity in human lung epithelial cell line (H1355). 4-Methoxyestradiol treatment significantly decreased cell growth and increased mitotic index. Elevation of ROS and SOD activity, with a concomitant decrease in the intracellular GSH/GSSG ratio, was also detected in 4-MeOE2-treated cells. Quantitative comet assay showed increased oxidative DNA damage in the 4-MeOE2-treated H1355 cells, which could be significantly reduced by the anti-oxidant N-acetylcysteine (NAC). However, inhibition of cell growth and increase in mitotic arrest induced by 4-MeOE2 were unaffected by NAC. We concluded that 4-MeOE2 accumulation resulting from TCDD and E-2 interaction would contribute to the higher vulnerability on lung pathogenesis in females when exposed to TCDD. (c) 2007 Elsevier Inc. All rights reserved.
    Keywords: Pharmacology & Pharmacy;Toxicology
    Date: 2007-05-01
    Relation: Toxicology and Applied Pharmacology. 2007 May;220(3):271-277.
    Link to: http://dx.doi.org/10.1016/j.taap.2007.01.024
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0041-008X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000246325600006
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34247212151
    Appears in Collections:[Pinpin Lin] Periodical Articles
    [Louis W. Chang(1999-2009)] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    000246325600006.pdf414KbAdobe PDF899View/Open


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

    Related Items in TAIR

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