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有氧运动协同抗氧化剂对老年小鼠肾脏线粒体质和量的影响 被引量:8

The Effect of Aerobic Training and Antioxidant on Renal Mitochondria in Quantity and Quality from Aged Mice
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摘要 目的:研究小鼠衰老时肾脏线粒体形态、结构、功能及mtDNA的变化规律,观察有氧运动训练和抗氧化剂延缓肾脏老化的效果。方法:用电镜对线粒体观察计数,Clark氧电极法测定线粒体呼吸链CytC氧化酶及NADH脱氢酶活性,分光光度法测定抗氧化酶活性,聚合酶链反应检测mtDNA3866bp片段缺失率。结果:与 5月龄小鼠比较, 20月龄的老年小鼠肾脏线粒体数量减少、体积增大,线粒体呼吸控制率、ADP/O比值减小,呼吸链NADH脱氢酶、CytC氧化酶活性下降,mtDNA3866bp片段缺失率增加,而抗氧化酶活性却增大。结论:长期进行有氧运动和 /或补充抗氧化剂可在一定程度上维持机体氧化与抗氧化的平衡,延缓mtDNA片段缺失率随增龄积累,预防线粒体老化,改善线粒体功能。 To investigate the changes of renal mitochondria morphology,function and antioxidant activity mitochondria of aged mice,and evaluate the protective effects of aerobic training and antioxidant on the aging course,Morphometric quantitative study of mitochondria in myocardium was investigated by electron microscopy cytochrome oxidase activities were measured polarogaphically with spectrophotography and clark oxygen electrode,levels of mtDNA deletion were determinded by polymerase chain reaction (PCR).It was found that decreased RCR,ADP/O,NADH hydrodase and cytochrome oxidase activities and abnormal size and structure of renal mitochondria were accompanied by a significantly increase antioxidant enzymes in aged mice,in the mean time,the 3866bp fragment deletion of mtDNA was increased.Adaptive changes of mitochondria were brought by aerobic training and antioxidant which might protect mtDNA from oxidative damage and delay the age-related decline of mitochondrial function in renal of aged mice.
作者 陈彩珍 卢健
出处 《成都体育学院学报》 CSSCI 北大核心 2005年第1期89-92,113,共5页 Journal of Chengdu Sport University
关键词 线粒体 肾脏 MTDNA 呼吸链酶 抗氧化剂 衰老 mitochondria renal mtDNA mitochondrial respiratory chain enzymes Antioxidant aging aerobic training
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  • 1Zhang C ,Liu VW,Addessi CL,et al. Difterential occurrence of muittions in mnochondrial DNA of human skeletal muscle during aging [ J ]. Hnm. Mutat, 1998,11 (5): 360 - 371.
  • 2Yowe DL, Ames BN. Quantitation of age - related mitochondrial DNA deletions in rat tissues showsthat their pattern of accumulation differs from that of humans [ J ]. Gene, 1998,209 (1 -2) :23 -30.
  • 3Tengan CH, Gabbai AA, Shanske S, et al. Oxidative phosphorylation dysfunction does not increase the rate of accumulation of age- related mitochondrial DNA deletions in skeletal musele [ J ].Mutat Res, 1997,379( 1 ) :1-11.
  • 4Shigenaga MK, Hagen TM, Ames BN. Oxidative damage and mitochondrial decay in aging [ J ]. Proe NatI Acad Sci USA,1994,91:10771 - 10778.
  • 5Zamora A J, Tessier F, Marconnet P. Mitochondria changes in human muscle after prolonged exercise, ecdurance training and selenium supplementation[J]. Eur J Appl Physiol, 1995,71:505 -511.
  • 6Scholz RW, Mrnicucci LA, Reddy CC. Effect of Vitamin E and Selenium on antioxidant defense in rat heart[ J ]. Biochem Mol Bioi Int, 1997,42 ( 5 ) :997-1006.
  • 7Gadaleta G,Pepe G, Candia G, et al. The complete nucleotide sequence of the Rattus norvegicus mitochondrial genome: Cryptic signals revealed by compsrative analysis between vertebrates [ J ].JMolEvol, 1989,28: 497 -516.
  • 8Bandy B, Darison AJ. Mitochondrial mutations may increase oxidative stress: Implications for carcinogenesis and ageing[ J ]. Free Radical Biol Med, 1990,8 :523 - 539.
  • 9Linnane AW, Marzuki S, Ozawa T, et al. Mitochondrial DNA mutations as an impotant contributor to ageing and degenerative disease[J]. Lancet ,1989, ( 1 ) :642 -645.
  • 10Sen CK. Antioxidant and redox regulation of gene transcription[J]. FASEB J,1996,10:709-720.

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