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氧化应激、线粒体通透性转换与肝衰竭的相关性

王克菲 朱跃科 孟庆华

引用本文:
Citation:

氧化应激、线粒体通透性转换与肝衰竭的相关性

DOI: 10.3969/j.issn.1001-5256.2013.09.021
基金项目: 

首都卫生发展科研专项项目(2011-2018-09); 北京市教育委员会科研计划项目(11320098); 北京市自然科学基金资助项目(7112064); 

详细信息
  • 中图分类号: R575.3

Research advances in oxidative stress and mitochondrial permeability transition in liver failure

Research funding: 

 

  • 摘要: 目前治疗肝衰竭的主要手段有内科综合治疗、人工肝治疗、肝移植和干细胞移植治疗,虽然取得了较好的疗效,但是仍然有一部分患者由于病情凶险及治疗时机延误而最终死亡。氧化应激损伤是近年来研究的热点,抗氧化治疗也越来越受到关注。综合近年来的研究成果,对氧化应激损伤、线粒体膜通透性转换孔(MPTP)线粒体膜通透性转换孔及其与肝衰竭疾病的相关性做综述,阐明氧化应激损伤在肝衰竭发病中的重要性,为今后的进一步抗氧化治疗提供理论依据及思路。

     

  • [1]Liver Failure and Artificial Liver Group, Chinese Society of Infectious Diseases, Chinese Medical Association.Diagnostic and treatment guidelines for liver failure[J].Chin J Hepatol, 2006, 14 (9) :643-646. (in Chinese) 中华医学会感染病学分会肝衰竭与人工肝学组, 中华医学会肝病学分会重型肝病与人工肝学组.肝衰竭诊疗指南[J].中华肝脏病杂志, 2006, 14 (9) :643-646.
    [2]KUMAR A, DAS K, SHARMA P, et al.Hemodynamic studies in acute-on-chronic liver failure[J].Dig Dis Sci, 2009, 54 (4) :869-878.
    [3]KHAN SA, SHAH N, WILLIAMS R, et al.Acute liver failure:a review[J].Clin Liver Dis, 2006, 10 (2) :239-258.
    [4]TURRENS JF.Superoxide production by the mitochondrial respiratory chain[J].Biosci Rep, 1997, 17 (1) :3-8.
    [5]WANG QL, WANG HY, WANG SR.Assessment of the state of oxidative stress[J].Chin J Pathophysiol, 2005, 21 (10) :2068-2074. (in Chinese) 王秋林, 王浩毅, 王树人, 等.氧化应激状态的评价[J].中国病理生理杂志, 2005, 21 (10) :2068-2074.
    [6]WITKO-SARSAT V, FRIEDLANDER M, CAPEIKKEREBLANDIN C, et al.Advanced oxidation protein products as a novel marker of oxidative stress in uremia[J].Kidney Into, 1996, 49 (5) :1304-1313.
    [7]LIU H, HAN T, TIAN J, et al.Monitoring oxidative stress in acute-on-chronic liver failure by advanced oxidation protein products[J].Hepatol Res, 2012, 42 (2) :171-180.
    [8]CHEN Y, YANG Y, MILLER ML, et al.Hepatocyte-specific Gclc deletion leads to rapid onset of steatosis with mitochondrial injury and liver failure[J].Hepatology, 2007, 45 (5) :1118-1128.
    [9]LIU J, TAN H, SUN Y, et al.The preventive effects of heparinsuperoxide dismutase on carbon tetrachloride-induced acute liver failure and hepatic fibrosis in mice[J].Mol Cell Biochem, 2009, 327 (1-2) :219-228.
    [10]BOSOI CR, ROSE CF.Oxidative stress:a systemic factor implicated in the pathogenesis of hepatic encephalopathy[J].Metab Brain Dis, 2013, 28 (2) :175-178.
    [11]BOVERIS A, CHANCE B.The mitochondrial generation of hydrogen peroxide.General properties and effect of hyperbaric oxygen[J].Biochem J, 1973, 134 (3) :707-716.
    [12]ST-PIERRE J, BUCKINGHAM JA, Roebuck SJ, et al.Topology of superoxide production from different sites in the mitochondrial electron transport chain[J].J Biol Chem, 2002, 277 (47) :44784-44790.
    [13]STANIEK K, NOHL H.Are mitochondria a permanent source of reactive oxygen species?[J].Biochim Biophys Acta, 2000, 1460 (2-3) :268-275.
    [14]LI F, SONVEAUX P, RABBANI ZN, et al.Regulation of HIF-1alpha stability through S-nitrosylation[J].Mol Cell, 2007, 26 (1) :63-74.
    [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]BEDARD K, KRAUSE KH.The NOX family of ROS-generating NADPH oxidases:physiology and path physiology[J].Physiol Rev, 2007, 87 (1) :245-313.
    [17]CHANDEL NS, MCCLINTOCK DS, Feliciano CE, et al.Reactive oxygen species generated at mitochondrial complex III stabilize hypoxia-inducible factor-1alpha during hypoxia:a mechanism of O2sensing[J].J Biol Chem, 2000, 275 (33) :25130-25138.
    [18]ALLEN RG, BALIN AK.Oxidative influence on development and differentiation:An overview of a free radical theory of development[J].Free Radic Biol Med, 1989, 6 (6) :631-661.
    [19]ANDREYEV AY, KUSHNAREVA YE, STARKOV AA.Mitochondrial metabolism of reactive oxygen species[J].Biochemistry (Mosc) , 2005, 70 (2) :200-214.
    [20]RHEE SG.Cell signaling.H2O2, a necessary evil for cell signaling[J].Science, 2006, 312 (5782) :1882-1883.
    [21]KINNALLY KW, PEIXOTO PM, RYU SY, et al.Is MPTP the gatekeeper for necrosis, apoptosis, or both?[J].Biochim Biophys Acta, 2011, 1813 (4) :616-622.
    [22]HAUSENLOY DJ, ONG SB, YELLON DM.The mitochondrial permeability transition pores as a target for preconditioning and post conditioning[J].Basic Res Cardiol, 2009, 104 (2) :189-202.
    [23]SIEMEN D, ZIEMER M.What is the nature of the mitochondrial permeability transition pore and what is it not?[J].IUBMB Life, 2013, 65 (3) :255-262.
    [24]HAWORTH RA, HUNTER DR.The Ca2+-induced membrane transition in mitochondria II.Nature of the Ca2+trigger site[J].Arch Biochem Biophys, 1979, 195 (2) :460-467.
    [25]BONORA M, BONONI A, De MARCHI E, et al.Role of the c subunit of the FO ATP syntheses in mitochondrial permeability transition[J].Cell Cycle, 2013, 12 (4) :674-683.
    [26]REUTENAUER J, DORCHIES OM, PATTHEY-VUADENS O, et al.Investigation of Debio 025, a cyclophilin inhibitor, in the dystrophic mdx mouse, a model for duchene muscular dystrophy[J].Br J Pharmacol, 2008, 155 (4) :574-584.
    [27]RAMACHANDRAN A, LEBOFSKY M, BAINES CP, et al.Cyclophilin D deficiency protects against acetaminophen-induced oxidant stress and liver injury[J].Free Radic Res, 2011, 45 (2) :156-164.
    [28]SUSIN SA, DAUGAS E, RAVAGNAN L, et al.Two distinct pathways leading to nuclear apoptosis[J].J Exp Med, 2000, 192 (4) :571-580.
    [29] PEIXOTO PM, RYU SY, DEJEAN LM.et al.Is MPTP the gatekeeper for necrosis, apoptosis, or both?[J].Biochim Biophys Acta, 2011, 813 (4) :616-622.
    [30]KANG KA, KIM JS, ZHANG R, et al.Induction of hemeoxygenase-1 by plant extract KIOM-79 via Akt pathway and NF-E2 related factor 2 in pancreatic beta-cells[J].J Toxicol Environ Health A, 2008, 71 (20) :1392-1399.
    [31]GALLUZZI L, MORSELLI E, KEPP O, et al.Mitochondrial gate ways to cancer[J].Mol Aspects Med, 2010, 31 (1) :1-20.
    [32]LIAO MY, ZHOU KJ, et al.Changes of mitochondrial permeability transition during rat liver regeneration[J].Acad J Second Military Med Univ, 2004, 25 (3) :292-294. (in Chinese) 缪明永, 朱克军, 汪振诚, 等.大鼠肝再生时线粒体通透性转换的变化[J].第二军医大学学报, 2004, 25 (3) :292-294.
    [33]BERNARDI P.Modulation of the mitochondrial cyclosporin Asensitive permeability transition pores by the proton electrochemical gradient.Evidence that the pore can be opened by membrane depolarization[J].J Biol Chem, 1992, 267 (13) :8834-8839.
    [34]BOUGHTON-SMITH NK, EVANS SM, LASZLO F, et al.The induction of nitric oxide synthase and intestinal vascular permeability by endotoxin in the rat[J].Br J Pharmacol, 1993, 110 (3) :1189-1195.
    [35]FANG H, CHEN M, DING Y, et al.Imaging superoxide flash and metabolism-coupled mitochondrial permeability transition in living animals[J].Cell Res, 2011, 21 (9) :1295-1304.
    [36]MA Q, FANG H, SHANG W, et al.Superoxide flashes:Early mitochondrial signals for oxidative stress-induced apoptosis[J].J Biol Chem, 2011, 286 (31) :27573-27581.
    [37]YANG J, LIU X, BHALLA K, et al.Prevention of apoptosis by Bcl-2:release of cytochrome c from mitochondria blocked[J].Science, 1997, 275 (5303) :1129-1132.
    [38]CHEN Q, CHAI YC, MAZUMDER S, et al.The late increase in intracellular free radical oxygen species during apoptosis is associated with cytochrome c release, caspase activation, and mitochondrial dysfunction[J].Cell Death Differ, 2003, 10 (3) :323-334.
    [39]CHORNA SV, DOSENKO VIE, STRUTYNS'KA NA, et al.Increased expression of voltage-dependent anion channel and adenine nucleotide translocase and the sensitivity of calcium-induced mitochondrial permeability transition opening pore in the old rat heart[J].Fiziol Zh, 2010, 56 (4) :19-25.
    [40]SCHRIEWER JM, PEEK CB, BASS J, et al.ROS-mediated PARP activity undermines mitochondrial function after permeability transition pore opening during myocardial ischemia-reperfusion[J].J Am Heart Assoc, 2013, 2 (2) :e000159.
    [41]GE ZC, XU HY, HOU WS, et al.Analysis of clinical characteristics and related factors affecting the prognosis of varies liver failure[J].J Clin Hepatol, 2009, 25 (5) :352-354. (in Chinese) 葛宗成, 许慧阳, 候为顺, 等.不同类型肝衰竭临床特点及其转归相关危险因素分析[J].临床肝胆病杂志, 2009, 25 (5) :352-354.
    [42]DUAN ZP, CHEN Y.Recent progress and future perspectives of liver failure diagnosis and treatment strategies[J].J Clin Hepatol, 2012, 28 (10) :721-725. (in Chinese) 段钟平, 陈煜.肝衰竭诊疗:进展与展望[J].临床肝胆病杂志, 2012, 28 (10) :721-725.
    [43]CHAPPELL JB, CROFTS AR.Calciumion accumulation and volume changes of isolated liver mitochondria.Calciumion-induced swelling.[J].Biochem J, 1965, 95:378-386.
    [44]SEN S, DAVIES NA, MOOKERJEE RP, et al.Path physiological effects of albumin dialysis in acute-on-chronic liver failure:a randomized controlled study[J].Liver Transpl, 2004, 10 (9) :1109-1119.
    [45]HIGUCHI M, AGGARWAL BB, YEH ET.Activation of CPP32-like protease in tumor necrosis factor-induced apoptosis is dependent on mitochondrial function[J].J Clin Invest, 1997, 99 (7) :1751-1758.
    [46]SCHULZE-OSTHOFF K, BAKKER AC, VANHAESEBROECK B, et al.Cytotoxic activity of tumor necrosis factor is mediated by early damage of mitochondrial functions[J].J Biol Chem, 1992, 267 (8) :5317-5323.
    [47]VALLANCE P, MONCADA S.Hyperdynamic circulation in cirrhosis:a role for nitric oxide?[J].Lancet, 1991, 337 (8744) :776-778.
    [48]HELMY A, JALAN R, NEWBY DE, et al.Altered peripheral vascular responses to exogenous and endogenous endothelin-1 in patients with well-compensated cirrhosis[J].Hepatology, 2001, 33 (4) :826-831.
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  • 收稿日期:  2013-03-21
  • 出版日期:  2013-09-20
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