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锰超氧化物歧化酶与糖尿病慢性并发症 被引量：3

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摘要 近年对糖尿病（DM）慢性并发症（chronic complications of diabetes mellitus，DCC）发病机制的研究显示，氧化应激在DM及其各种DCC中起着不容忽视的作用，成为发病机制研究中的一个热点。而锰超氧化物歧化酶（Mn-superoxide dismutase，Mn-SOD）作为线粒体内的抗氧化酶，对抗氧化损伤起着重要作用，一些学者已经注意到Mn-SOD在线粒体内的活性下降与许多疾病包括DCC在内的相关性。
作者 王文霞 贾伟平
机构地区 上海交通大学附属第六人民医院
出处 《上海医学》 CAS CSCD 北大核心 2006年第4期257-259,共3页 Shanghai Medical Journal
关键词 糖尿病慢性并发症 锰超氧化物歧化酶 糖尿病(DM) 发病机制研究 MN-SOD 线粒体内 抗氧化损伤 氧化应激 抗氧化酶 DCC
分类号 R587.2 [医药卫生—内分泌] R739.5 [医药卫生—肿瘤]
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参考文献20

  • 1Ikegami T, Suzuki Y, Shimizu T, et al. Model mice for tissue-specific deletion of the manganese superoxide dismutase(MnSOD) gene. Biochem Biophys Res Commun, 2002,296:729-736
  • 2Lortz S,Tiedge M. Sequential inactivation of reactive oxygen species by combined overexpression of SOD isoforms and catalase in insulin-producing cells. Free Radic Biol Med,2003,34:683-688.
  • 3Su SB, Motoo Y,Xie MJ,et al. Superoxide dismutase is induced during rat pancreatic acinar cell injury. Pancreas,2002,24: 146-152.
  • 4Jones SP, Hoffmeyer MR, Sharp BR, et al. Role of intracellular antioxidant enzymes after in vivo myocardial ischemia and reperfusion. Am J Physiol Heart Circ Physiol, 2003, 284:H277-H282.
  • 5Yan C, Huang A, Wu Z, et al. Increased superoxide leads to decreased flow-induced dilation in resistance arteries of Mn-SOD-deficient mice. Am J Physiol Heart Circ Physiol, 2005,288 : H2225-H2231.
  • 6Nishikawa T, Edelstein D, Du XL, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature, 2000, 404:787-790.
  • 7Stadler K, Jenei V, von Bolcshazy G, et al. Role of free radicals and reactive nitrogen species in the late complications of diabetes mellitus in rats. Orv Hetil, 2004,145 : 1135-1140.
  • 8Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature, 2001, 414:813-820.
  • 9Feldman EL. Oxidative stress and diabetic neuropathy: a new understanding of an old problem. J Clin Invest, 2003, 111:431-433.
  • 10Shaw S, Wang X, Redd H, et al. High glucose augments the angiotensin Ⅱ-induced activation of JAK 2 in vascular smooth muscle cells via the polyol pathway. J Biol Chem,2003, 278 : 30634-30641.

二级参考文献8

  • 1TAKASHI N, YASUSHI T, LIANSHAN P, et al.The polymorphism of manganese superoxide dismutase is associated with diabetic nephropathy in Japanese type 2 diabetic patients [ J ]. J Hum Genet, 2003,48: 138.
  • 2CHISTYAKOV D A, SAVOST′ANOV K V, ZOTOVA E V, et al. Polymorphisms in the Mn- SOD and ECSOD genes and their relationship to diabetic neuropathy in type 1 diabetes mellitus[J]. BMC Med Genet, 2001, 2:4.
  • 3COWIE C C, PORT F K, WOLFE R A, et al. Disparities in incidence of diabetic end - stage renal disease according to race and type of diabetes [ J ]. N Engl J Med, 1982, 321:1074.
  • 4DIABETES DRAFTING GROUP. Prevalence of small vessel and large vessel disease in diabetic patients from 14centres: the world health organization multinational study of vascular disease in diabetics[J]. Diabetologia, 1986,28 (Suppl): 615.
  • 5PARK J Y, KIM H K, CHUNG Y E, et al. Incidence and determinants of microalbuminuria in Koreanswith type 2 diabetes [J]. Diabetes Care, 1998,21 (4) 530.
  • 6VAN LANDEGHEM G F, TABATABAIE P,KUCINSKASV, et al. Ethnic variation in the mitochondrial targeting sequence polymorphism of MnSOD[J]. Hum Hered, 1999, 49:190.
  • 7HORI H, HARADA H, NISHI H, et al. Polymorphisms in the SOD2 and HLA- DRBi genes are associated with nonfamilial idiopathle dilated cardiomyopathy in Japanese[J].Biochem Biophys Res Commun, 1999, 261:332.
  • 8杨金奎,谌贻璞.糖尿病肾病诊治研究进展[J].基础医学与临床,2003,23(4):353-358. 被引量：20

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二级引证文献28

上海医学
2006年 第4期

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