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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/26717


    標題: Oxidative stress and pyrogenic fever pathogenesis
    作者: Hou, Ching-Cheng
    Lin, Hung
    Chang, Ching-Ping
    Huang, Wu-Tein
    Lin, Mao-Tsun
    貢獻者: 休閒保健管理系
    關鍵字: Pyrogen
    Fever
    Glutamate
    Nitric oxide metabolite
    Hydroxyl radical
    日期: 2011-09
    上傳時間: 2013-06-21 16:52:29 (UTC+8)
    出版者: Elsevier
    摘要: The causative/regulatory connections between changes in tissue redox state and fever induction were investigated herein. Wherefore, LPS, the primary element of bacterial cell wall, in addition to inducing pro-inflammatory cytokines, activated macrophages and other leukocytes to secrete hydroxyl radical (OH), nitric oxide metabolites (NOx−), superoxide (O2) and other reactive oxygen/nitrogen species. Furthermore, inflammation response-associated hypoxia stimulated glutamate release, which caused excitotoxicity of cells by increasing extracellular Ca2+. Cytokines and glutamate in turn also triggered the release of large amounts of NOx−, OH, O2, and other radicals. Those reactive nitrogen species in turn caused cellular injury via the peroxidation of membrane lipids and oxidative damage of proteins and DNA. Glutamate, NOx−, OH and antioxidants participated in the pathogenesis and regulation of LPS- or cytokines-induced fever. In particular, to highlight the role of glutamate, prostaglandin E2, NOx− and OH generated in the hypothalamus during pyrogenic fever was attempted hereby. To find the link among the signaling with the glutamate, NOx− and OH/prostaglandin E2 in the hypothalamus during pyrogenic fever will be challenging and could now clinically suppress pyrogenic fever.
    Appears in Collections:[休閒保健管理系(所)] 期刊論文

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