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当机体的氧化作用与抗氧化作用失衡并向氧化作用倾斜时,机体产生氧化应激(oxidative stress).氧化应激可促进活性氧簇(reactive oxygen species,ROS)和活性氮簇(reactive nitrogen species,RNS)等的产生[1].产生的活性氧簇和活性氮簇不仅损伤核酸、蛋白质、脂质等生物分子以及线粒体等细胞器,还作为信使分子参与调节基因表达等生理病理过程,进而对细胞或机体组织产生损伤. 相似文献
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需氧生物体在正常生理代谢过程中会产生活性氧族(reactive oxygen species,ROS),但过多的ROS可引起体内多种氧化损伤,因此这类生物体都具备一套完善的防御体系,抗氧化酶是其中一个重要的组成部分。对于医学吸虫,不仅需要抗氧化酶清除正常生理代谢中产生的ROS,还要抵抗宿主免疫系统来源的ROS引起的损伤。了解医学吸虫抗氧化酶家族的结构和特性,有助于对其生殖生理的研究,以及新型药物和疫苗的开发。本文综述近年来对医学吸虫谷胱甘肽过氧化物酶(glutathione peroxidase,GPx)、超氧化物歧化酶(superoxide dismutase,SOD)及抗氧化蛋白(peroxire-doxin,PRx)等抗氧化酶家族的研究进展。 相似文献
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杜学海 《肾脏病与透析肾移植杂志》1992,(2)
一、反应性氧代谢产物的形成反应性氧代谢产物(reactive oxygenmetabolites,ROM)或反应性氧族(reactiveoxygen species,ROS),是超氧阴离子(O_2~-)、过氧化氢(H_2O_2)、羟自由基(.OH)、单线氧(′O_2)和次氯酸(来自髓过氧化物酶-H_2O_2-卤化物系统)的总称。 相似文献
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氧化应激和抗氧化治疗在慢性肾功能衰竭和高血压中的作用 总被引:5,自引:0,他引:5
氧化应激是指由于活性氧(reactive oxygen species,ROS)过度产生与抗氧化防御机制减弱两者平衡失调造成的组织损伤。ROS包括过氧化氢和氢氧化物自由基等是在氧代谢过程中产生的正常中间代谢产物。ROS可以与蛋白质、脂肪、核酸、碳水化合物以及其他分子发生强烈反应并使之变性,引起炎症反应、凋亡、纤维化和细胞增殖。因此,在正常情况下,ROS作为单分子起着极其重要的作用,ROS的产生是炎症反应和组织损伤修复过程的重要生理步骤。 相似文献
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抗氧化剂酶在保护线虫和吸虫兔受反应性氧族ROS损伤中具有重要作用,也有些虫种虽缺乏代谢过氧化氢的触酶及谷胱甘肽过氧化物酶(GPX),但仍有高水平的超氧化物酶(SOD)活性,近来认为硫氧还蛋白过氧化物酶(thioredoxin peroxidase,TPx)可能是ROS代谢中未被发现的重要环节。TPx是一 相似文献
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糖尿病、高血压、高脂血症等病理状态下,由于细胞正常的氧化还原稳态失衡,活性氧族(reactive oxygen species,ROS)过度产生而聚积,引起氧化应激。研究表明,氧化应激能引起内皮祖细胞(endothelial progenitor cells,EPCs)的数量减少,影响EPCs的动员、迁移、增殖及分化功能。EPCs能参与血管内皮的新生,对糖尿病血管病变有保护作用。故从某种意义上讲,外周循环中EPCs的数量和功能决定损伤 相似文献
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《胃肠病学和肝病学杂志》2016,(8)
氧气吸入是治疗一些疾病的重要手段,尤其可改善新生儿缺氧状态。但长时间的高氧治疗会对机体器官产生严重的毒性作用。高氧能诱发线粒体产生活性氧(reactive oxygen species,ROS)进而引起器官损伤。高氧环境中肠上皮细胞遭到破坏时伴随着ROS的增加,激活NF-κB信号通路,进而引起一系列的炎症反应,因此,ROS在高氧肠道损伤中发挥着重要作用。 相似文献
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Peroxiredoxin(Prx)属于一个广泛存在的过氧化物酶家族,对许多病原体在有氧环境下的生存起重要作用。该文综述了Prx的结构、分类及其在寄生性原虫中的研究进展。 相似文献
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氧还蛋白过氧化物酶 (Peroxiredoxin, Prx) 广泛存在于酵母、 真菌、 寄生虫、 哺乳动物和人类等多种生物体, 是过氧化物酶家族重要的抗氧化蛋白之一。Prx可以抵抗生物体内产生的活性氧分子和活性氮分子, 在生物体内起着重要的抗氧化作用。本文综述了Prx的分类、 作用机制, 以及无脊椎动物Prx的研究进展。 相似文献
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研究发现活性氧与男性不育具有一定相关性,如何预防过量活性氧的产生和清除过量的活性氧是近年研究的热点之一。该文主要综述活性氧对精子的生理及病理作用、精液活性氧的来源及检测方法、活性氧对辅助生殖的影响等方面的相关研究进展。 相似文献
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过氧化物还原酶(Prx)是高度保守的过氧化物酶。Prx的硫氧还蛋白过氧化物酶的活性对维持低水平内源性过氧化氢具有重要意义,并有促进过氧化氢介导的信号功能。丝裂原活化蛋白激酶(MAPK)信号途径介导细胞对包括活性氧(ROS)在内的多种刺激作出反应。文章在此总结Prx可以在MAPK的激活中同时扮演传感器和障碍的证据,并讨论所涉及的具体机制,特别是其与硫氧还蛋白(Trx)的关系。 相似文献
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Peroxiredoxins (Prx) are a family of anti‐oxidants that protect cells from metabolically produced reactive oxygen species (ROS). The presence of these enzymes in the secretomes of many parasitic helminths suggests they provide protection against ROS released by host immune effector cells. However, we recently reported that helminth‐secreted Prx also contribute to the development of Th2‐responses via a mechanism involving the induction of alternatively activated macrophages. In this review, we discuss the role helminth Prx may play in modulating the immune responses of their hosts. 相似文献
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Bae SH Sung SH Cho EJ Lee SK Lee HE Woo HA Yu DY Kil IS Rhee SG 《Hepatology (Baltimore, Md.)》2011,53(3):945-953
Peroxiredoxins (Prxs) are peroxidases that catalyze the reduction of reactive oxygen species (ROS). The active site cysteine residue of members of the 2-Cys Prx subgroup (Prx I to IV) of Prxs is hyperoxidized to cysteine sulfinic acid (Cys-SO(2) ) during catalysis with concomitant loss of peroxidase activity. Reactivation of the hyperoxidized Prx is catalyzed by sulfiredoxin (Srx). Ethanol consumption induces the accumulation of cytochrome P450 2E1 (CYP2E1), a major contributor to ethanol-induced ROS production in the liver. We now show that chronic ethanol feeding markedly increased the expression of Srx in the liver of mice in a largely Nrf2-dependent manner. Among Prx I to IV, only Prx I was found to be hyperoxidized in the liver of ethanol-fed wildtype mice, and the level of Prx I-SO(2) increased to ≈30% to 50% of total Prx I in the liver of ethanol-fed Srx(-/-) mice. This result suggests that Prx I is the most active 2-Cys Prx in elimination of ROS from the liver of ethanol-fed mice and that, despite the up-regulation of Srx expression by ethanol, the capacity of Srx is not sufficient to counteract the hyperoxidation of Prx I that occurs during ROS reduction. A protease protection assay revealed that a large fraction of Prx I is located together with CYP2E1 at the cytosolic side of the endoplasmic reticulum membrane. The selective role of Prx I in ROS removal is thus likely attributable to the proximity of Prx I and CYP2E1. CONCLUSION: The pivotal functions of Srx and Prx I in protection of the liver in ethanol-fed mice was evident from the severe oxidative damage observed in mice lacking either Srx or Prx I. 相似文献
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大黄素诱导肝癌细胞氧化损伤的实验研究 总被引:5,自引:0,他引:5
目的:研究大黄素抑制肝癌细胞增殖的作用机理。方法:采用流式细胞仪法观察了大黄素对肝癌细胞内活性氧的影响;采用MTT比色法观察了大黄素对细胞增殖的影响。结果:大黄素作用于肝癌细胞后,在2小时内引起活性氧的产生;大黄素抑制了肝癌细胞的增殖。结论:大黄素能够通过诱导细胞内活性氧的产生,引起细胞脂质过氧化,抑制了肝癌细胞的增殖。 相似文献
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Hemoglobin induces colon cancer cell proliferation by release of reactive oxygen species 总被引:1,自引:0,他引:1
INTRODUCTION Colon cancer is an important public health issue[1]. There are nearly one million cases of colon cancer diagnosed worldwide each year. The increasing trend of this cancer is prominent in Asian countries, including Korea[2,3]. Until the presen… 相似文献
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Summary Biphosphonates suppress bone destruction in various diseases. Several studies have demonstrated the potential use of biphosphonates in arthritis. The results of these studies indicate that the effectiveness of the biphosphonates, for inhibiting the arthritic process, is related to their antiresorptive properties. It has been shown that the generation of reactive oxygen species is associated with the formation of new osteoclasts and enhanced bone resorption. We studied the effects of the dichloromethylene diphosphonate on the reactive oxygen species production by activated polymorphonuclear leucocytes, measured by chemiluminescence. Our results indicate a dose-dependent inhibitory effect of dichloromethylene diphosphonate on reactive oxygen species production by polymorphonuclear leucocytes stimulated with N-formil-methionyl-leucyl-phenylalanine, the calcium ionophore A23187 and phorbol myristate acetate. The mechanisms by which this biphosphonate inhibits the reactive oxygen species production by activated polymorphonuclear leucocytes are discussed. 相似文献