我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

心肌细胞活性氧产生途径

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2018年第2期
页码:
240-243
栏目:
综述
出版日期:
2018-02-15

文章信息/Info

Title:
Reactive oxygen species production in cardiomyocytes
作者:
黄章泷12雷 霆2常 宇1
(1.北京工业大学生命科学与生物工程学院,北京 100124;2.北京深迈瑞医疗电子技术研究院有限公司,北京 100085)
Author(s):
HUANG Zhang-long12 LEI Ting2 CHANG Yu12
(1.College of Life Science and Bio-engineering, Beijing University of Technology, Beijing 100124, China; 2.Beijing Shen Mindray Medical Electronics Technology Co., LTD, Beijing 100085, China)
关键词:
心肌细胞活性氧线粒体电子传递链
Keywords:
Heart reactive oxygen species mitochondria electron transfer chain
分类号:
R329.2
DOI:
-
文献标识码:
A
摘要:
活性氧簇(ROS)是一类含氧的自由基或者非自由基分子,具有非常高的生物化学反应活性,能够与生物体内的蛋白质、脂质和DNA发生反应。ROS在正常的生理功能和心脏疾病的发生中均扮演着重要的角色,因此了解心肌细胞ROS的产生对心脏研究有积极意义。本文将综述心肌细胞ROS产生的位点及途径。
Abstract:
Reactive oxygen species (ROS) are a class of oxygen-containing free radicals or non radical molecules, which are so highly reactive that they can react with proteins, lipids and DNA in organisms. ROS play pivotal roles in the heart under both physiological and pathophysiological conditions, so understanding the production process of reactive oxygen species in cardiac cells is important to cardiac research. This review summarizes main ROS production pathways in cardiomyocytes.

参考文献/References

[1]Li C,Jackson RM.Reactive species mechanisms of cellular hypoxia-reoxygenation injury[J].Am J Physiol Cell Physiol,2002,282(2):C227-C241.

[2]Dhalla NS,Temsah RM,Netticadan T.Role of oxidative stress in cardiovascular diseases[J].J Hypertens,2000,18(6):655-673.

[3]Lonn E,Bosch J,Yusuf S,et al.Effects of long-term vitamin E supplementation on cardiovascular events and cancer:a randomized controlled trial[J].JAMA,2005,293(11):1338-47.

[4]Yan Y,Liu J,Wei C,et al.Bidirectional regulation of Ca2+ sparks by mitochondria-derived reactive oxygen species in cardiac myocytes[J].Cardiovasc Res,2008,77(2):432-441.

[5]Zhao Z,Wen H,Fefelova N,et al.Revisiting the ionic mechanisms of early afterdepolarizations in cardiomyocytes:predominant by Ca waves or Ca currents?[J].Am J Physiol Heart Circ Physiol,2012,302(8):H1636-H1644.

[6]Rajasekaran NS,Connell P,Christians ES,et al.Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice[J].Cell,2007,130(3):427-439.

[7]Owusu-Ansah E,Banerjee U.Reactive oxygen species prime Drosophila haematopoietic progenitors for differentiation[J].Nature,2009,461(7263):537-541.

[8]Maryanovich M,Gross A.A ROS rheostat for cell fate regulation[J].Trends Cell Biol,2012,23(3):129-134.

[9]Adler V,Yin Z,Tew KD,et al.Role of redox potential and reactive oxygen species in stress signaling[J].Oncogene,1999,18(45):6104-6111.

[10]Yoo SK,Starnes TW,Deng Q,et al.Lyn is a redox sensor that mediates leukocyte wound attraction in vivo[J].Nature,2011,480(7375):109-112.

[11]Valko M,Leibfritz D,Moncol J,et al.Free radicals and antioxidants in normal physiological functions and human disease[J].Int J Biochem Cell Biol,2007,39(1):44-84.

[12]Bashan N,Kovsan J,Kachko I,et al.Positive and negative regulation of insulin signaling by reactive oxygen and nitrogen species[J].Physiol Rev,2009,89(1):27-71.

[13]Turrens JF.Mitochondrial formation of reactive oxygen species[J].J Physiol,2003,552(Pt2):335-344.

[14]Dr?ge W.Free radicals in the physiological control of cell function[J]. Physiol Rev,2002,82(1):47-95.

[15]Nohl H,Gille L,Staniek K.The mystery of reactive oxygen species derived from cell respiration[J].Acta Biochim Pol,2004,51(1):223-229.

[16]Cadenas E,Boveris A,Ragan CI,et al.Production of superoxide radicals and hydrogen peroxide by NADH-ubiquinone reductase and ubiquinol-cytochrome c reductase from beef-heart mitochondria[J].Arch Biochem Biophys,1977,180(2):248-257.

[17]Takeshige K,Minakami S.NADH- and NADPH-dependent formation of superoxide anions by bovine heart submitochondrial particles and NADH-ubiquinone reductase preparation[J].Biochem J,1979,180(1):129-135.

[18]Kang D,Narabayashi H,Sata T,et al.Kinetics of superoxide formation by respiratory chain NADH-dehydrogenase of bovine heart mitochondria[J].J Biochem,1983,94(4):1301-1306.

[19]Genova ML,Pich MM,Biondi A,et al.Mitochondrial production of oxygen radical species and the role of Coenzyme Q as an antioxidant[J].Exp Biol Med(Maywood),2003,228(5):506-513.

[20]Korshunov SS,Skulachev VP,Starkov AA.High protonic potential actuates a mechanism of production of reactive oxygen species in mitochondria[J].FEBS Lett,1997,416(1):15-18.

[21]Krishnamoorthy G,Hinkle PC.Studies on the electron transfer pathway,topography of iron-sulfur centers, and site of coupling in NADH-Q oxidoreductase[J].J Biol Chem,1988,263(33):17566-17575.

[22]Kushnareva Y,Murphy AN,Andreyev A.Complex I-mediated reactive oxygen species generation:modulation by cytochrome c and NAD(P)+ oxidation-reduction state[J].Biochem J,2002,368(Pt 2):545-553.

[23]Starkov AA,Fiskum G.Regulation of brain mitochondrial H2O2 production by membrane potential and NAD(P)H redox state[J].J Neurochem,2003,86(5):1101-1107.

[24]Rich PR,Bonner WD.The sites of superoxide anion generation in higher plant mitochondria[J].Arch Biochem Biophys,1978,188(1):206-213.

[25]Ksenzenko M,Konstantinov AA,Khomutov GB,et al.Relationships between the effects of redox potential, alpha-thenoyltrifluoroacetone and malonate on O(2) and H2O2 generation by submitochondrial particles in the presence of succinate and antimycin[J].FEBS Lett,1984,175(1):105-108.

[26]Whatley SA,Curti D,Das Gupta F,et al.Superoxide,neuroleptics and the ubiquinone and cytochrome b5 reductases in brain and lymphocytes from normals and schizophrenic patients[J].Mol Psychiatry,1998,3(3):227-237.

[27]Hauptmann N,Grimsby J,Shih JC,et al.The metabolism of tyramine by monoamine oxidase A/B causes oxidative damage to mitochondrial DNA[J].Arch Biochem Biophys,1996,335(2):295-304.

[28]Loffler M,Becker C,Wegerle E,et al.Catalytic enzyme histochemistry and biochemical analysis of dihydroorotate dehydrogenase/oxidase and succinate dehydrogenase in mammalian tissues, cells and mitochondria[J].Histochem Cell Biol,1996,105(2):119-128.

[29]Miwa S,St-Pierre J,Partridge L,et al.Superoxide and hydrogen peroxide production by Drosophila mitochondria[J].Free Radic Biol Med,2003,35(8):938-48.

[30]Mclennan HR,Degli Esposti M.The contribution of mitochondrial respiratory complexes to the production of reactive oxygen species[J].J Bioenerg Biomembr,2000,32(2):153-162.

[31]Vasquez-Vivar J,Kalyanaraman B,Kennedy MC.Mitochondrial aconitase is a source of hydroxyl radical.An electron spin resonance investigation[J].J Biol Chem,2000,275(19):14064-14069.

[32]Tretter L,Adam-Vizi V.Generation of reactive oxygen species in the reaction catalyzed by alpha-ketoglutarate dehydrogenase[J].J Neurosci,2004,24(36):7771-7778.

[33]Sugamura K,Keaney JF Jr.Reactive oxygen species in cardiovascular disease[J].Free Radic Biol Med,2011,51(5):978-992.

备注/Memo

备注/Memo:
收稿日期:2016-12-19.基金项目:国家自然科技基金项目资助(91430215) 通讯作者:常宇,教授,主要从事人工心脏和心血管方面的研究 Email:changyu@bjut.edu.cn 作者简介:黄章泷,博士后 Email:bio_hzl@126.com
更新日期/Last Update: 1900-01-01