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    Please use this identifier to cite or link to this item: https://ir.fy.edu.tw:8080/ir/handle/987654321/9628


    Title: Zinc at pharmacologic concentrations affects cytokine expression and induces apoptosis of human peripheral blood mononuclear cells.
    Authors: Kee-Lung Chang;Thu-Ching Hung;Bau-Shan Hsieh;Yen-Hui Chen;Te-Fu Chen;Hsiao-Ling Cheng
    Contributors: 輔英科技大學 健康美容學位學程
    Keywords: Zinc;Cytokines, Apoptosis;Caspase-3;Nuclear factor-κB;c-fos
    Date: 2006-05-01
    Issue Date: 2010-11-11 11:21:43 (UTC+8)
    Abstract: Objective
    The present study examined the effect of zinc at concentrations of the apoptotic signaling pathway and immune function of peripheral blood mononuclear cells (PBMCs).

    Methods
    PBMCs from healthy subjects were treated in vitro with various zinc concentrations to imitate different serum statuses of physiologic (2 to 15 μM) and pharmacologic (15 to 100 μM) concentrations to higher than 100 μM and analyzed their expressions of cytokines and apoptotically related factors.

    Results
    Although a normal physiologic concentration of zinc had no effect on immunologic function or apoptosis of PBMCs, a pharmacologic concentration (100 μM) or higher affected both functions. Zinc decreased cell proliferation at concentrations higher than 100 μM and stimulated cytokine expression at concentrations of at least 100 μM. Further, at concentrations of at least 100 μM, apoptosis was induced, and expressions of caspase-3 and proapoptotic genes, including Fas (FasL) and c-fos, which trigger apoptosis through receptor-mediated extrinsic and mitochondrion-mediated apoptotic pathways, respectively, were increased. At concentrations at least 300 μM, expressions of antiapoptotic factors nuclear factor-κB, Bcl-2, and Bcl-XL were markedly decreased.

    Conclusions
    Zinc stimulates cytokine expression and induces apoptosis of PBMCs from healthy subjects only at concentrations equal to or greater than the serum pharmacologic range. Receptor-mediated extrinsic and mitochondrial-mediated intrinsic pathways are involved in this zinc-induced apoptosis.
    Relation: Nutrition 22(5),465-474
    Appears in Collections:[健康美容系] 期刊論文

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