内分泌
词汇介绍
拓展阅读
解析
Glutathione 英 /,gluːtə'θaɪəʊn/ 美 /,ɡlʊtə'θaɪ,on/
释 义 n. [生化] 谷胱甘肽
例 句 This is another source of immune-strengthening glutathione.这是另一种增强免疫的谷胱甘肽食物。
Reductase 英 /rɪ'dʌkteɪz/ 美 /rɪ'dʌktez/
释 义 n. [生化] 还原酶
同根词 reductive adj. 还原的；减少的
reducern. [助剂] 还原剂；减径管
例 句 In conjunction with the glutathione reductase/peroxidase system, NADPH maintains the sulfhydryl groups of globin in their reduced state.NADPH通过与谷胱甘肽还原酶/过氧化物酶系统结合，维持球蛋白巯基基团的还原态。
概述
概述
谷胱甘肽还原酶（GR），也称为谷胱甘肽二硫化物还原酶（GSR），在人中由GSR编码基因。谷胱甘肽还原酶（EC 1.8.1.7）催化将谷胱甘肽二硫键（GSSG）还原为巯基形式的谷胱甘肽（GSH），这是抵抗氧化应激和维持细胞还原环境的关键分子。谷胱甘肽还原酶是保守的。
功能
谷胱甘肽在维持人体细胞的正常功能和防止氧化应激方面起着关键作用。它可以清除羟自由基，单态氧和各种亲电试剂。还原型谷胱甘肽可减少谷胱甘肽过氧化物酶的氧化形式，从而减少过氧化氢（H2O2），这是细胞内一种危险的反应性物质。此外，它在异生物素的代谢和清除中起关键作用，在某些排毒酶中充当辅因子，参与转运，并将抗氧化剂（如维生素E和C）再生为它们的反应形式。细胞中存在的GSSG / GSH的比例是正确维持细胞氧化平衡的关键因素，也就是说，细胞必须维持高水平的还原型谷胱甘肽和低水平的氧化型谷胱甘肽二硫化物。谷胱甘肽还原酶维持这种狭窄的平衡，该酶催化GSSG还原为GSH。
缺乏症
谷胱甘肽还原酶缺乏症是一种罕见的疾病，其中红细胞，白细胞或两者均不存在谷胱甘肽还原酶活性。在一项研究中，在30年的过程中进行的15,000次谷胱甘肽还原酶缺乏症测试中，仅在2例中观察到了这种疾病。在同一项研究中，一名患者及其家人的谷胱甘肽还原酶缺乏症与白内障和迷走神经相关，另一名患者与严重的未结合高胆红素血症相关。有人提出，谷胱甘肽氧化还原系统（谷胱甘肽还原酶是其中的一部分）几乎完全负责保护眼晶状体细胞免受过氧化氢，因为这些细胞缺乏过氧化氢酶（一种催化过氧化氢分解的酶）和谷胱甘肽还原酶，而缺乏的个体白内障发生率很高。
由于未在饮食中摄入足够的核黄素，一些患者的谷胱甘肽活性水平低下。核黄素是FAD的前体，其还原形式向二硫键提供两个电子，二硫键以谷胱甘肽还原酶的氧化形式存在，以开始酶的催化循环。1999年，一项研究发现，由于核黄素缺乏，在沙特阿拉伯检查的男性中17.8%的女性和22.4%的女性具有低谷胱甘肽还原酶活性。
Dimethyl Fumarate Induces Glutathione Recycling by Upregulation of Glutathione Reductase
复制标题
富马酸二甲酯通过谷胱甘肽还原酶的上调诱导谷胱甘肽再循环
发表时间：2017-01-01
影响指数：4.9
作者： Christina Hoffmann
期刊：Oxid Med Cell Longev
While an increasing number of therapeutic options have been developed to prevent the acute inflammatory insults in multiple sclerosis (MS) there is an urgent need for an effective treatment for the chronic neuronal degeneration occurring afterwards. This is of special importance as this degeneration is thought to be a major factor driving the development of chronic disability in these patients. A promising target for therapeutic interventions is oxidative stress which is prominently involved in neurodegeneration in MS. Dimethyl fumarate (DMF) is an effective oral therapeutic, which reduces disease activity and progression in patients with relapsing-remitting MS and psoriasis. DMF and its active metabolite monomethyl fumarate (MMF) exert a number of immunomodulatory effects involving increased apoptosis of T cells stimulated with interleukin- (IL-) 2 or anti-CD3 antibodies, inhibition of translocation to the nucleus of the nuclear factor kappa B1/p50 (NF-kB1) induced by the cytokines tumor necrosis factor α and IL-1α， and an increased production of protective T helper 2 cytokines IL-4 and IL-5 in CD2/CD8 monoclonal antibody stimulated peripheral blood mononuclear cells. Besides these immunomodulatory actions, DMF has a prominent antioxidative activity; it first induces short-lived oxidative stress by scavenging the major intracellular antioxidant glutathione (GSH). This results in stabilization and increased levels of the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) by means of Kelchlike ECH-associated protein 1 (KEAP1) which normally targets Nrf2 for ubiquitination and degradation but loses this ability in response to electrophiles and oxidants. NRF2 then translocates to the nucleus and binds to antioxidant response elements in the promoters of protective genes such as heme-oxygenase-1 and NADPH-quinoneoxidoreductase-1 (NQO1). This in turn increases the intracellular concentration of GSH, rendering the cells more resistant to oxidative stress.
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