English  |  正體中文  |  简体中文  |  Items with full text/Total items : 51948/87093 (60%)
Visitors : 8507339      Online Users : 290
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library & TKU 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://tkuir.lib.tku.edu.tw:8080/dspace/handle/987654321/97569


    Title: Nitric Oxide Physiological Responses and Delivery Mechanisms Probed by Water-Soluble Roussin’s Red Ester and {Fe(NO)2}10 DNIC
    Authors: Chen, Yi-Ju;Ku, Wei-Chi;Feng, Li-Ting;Tsai, Ming-Li;Hsieh, Chung-Hung;Hsu, Wen-Hwei;Liaw, Wen-Feng;Hung, Chen-Hsiung;Chen, Yu-Ju
    Contributors: 淡江大學化學學系
    Date: 2008-08
    Issue Date: 2014-03-27 09:17:43 (UTC+8)
    Publisher: Washington, DC: American Chemical Society
    Abstract: Dinitrosyl−iron complexes (DNICs) are stable carriers for nitric oxide (NO), an important biological signaling molecule and regulator. However, the insolubility of synthetic DNICs, such as Roussin’s red ester (RRE), in water has impaired efforts to unravel their biological functions. Here, we report a water-soluble and structurally well-characterized RRE [Fe(μ-SC2H4COOH)(NO)2]2 (DNIC-1) and a {Fe(NO)2}10 DNIC [(PPh2(Ph-3-SO3Na))2Fe(NO)2] (DNIC-2), their NO-induced protein regulation, and their cellular uptake mechanism using immortalized vascular endothelial cells as a model. Compared with the most common NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), the in vitro NO release assay showed that both DNICs acted as much slower yet higher stoichiometric NO-release agents with low cytotoxicity (IC50 > 1 mM). Furthermore, l-cysteine facilitated NO release from SNAP and DNIC-1, but not DNIC-2, in a dose- and time-dependent manner. EPR spectroscopic analysis showed, for the first time, that intact DNIC-1 can either diffuse or be transported into cells independently and can transform to either paramagnetic protein bound DNIC in the presence of serum or [DNIC-(Cys)2] with excess l-cysteine under serum-free conditions. Both DNICs subsequently induced NO-dependent upregulation of cellular heat shock protein 70 and in vivo protein S-nitrosylation. We conclude that both novel water-soluble DNICs have potential to release physiologically relevant quantities of NO and can be a good model for deciphering how iron−sulfur−nitrosyl compounds permeate into the cell membrane and for elucidating their physiological significance.
    Relation: Journal of the American Chemical Society 130(33), pp.10929-10938
    DOI: 10.1021/ja711494m
    Appears in Collections:[化學學系暨研究所] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML117View/Open

    All items in 機構典藏 are protected by copyright, with all rights reserved.


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