中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (11): 2063-2066.doi: 10.3969/j.issn.1673-8225.2012.11.038

• 组织构建基础实验 basic experiments in tissue construction • 上一篇    下一篇

线粒体生物学性状及细胞衰老和运动的影响*★

付  玉,王文迪,许苏旸,苏全生   

  1. 成都体育学院运动医学系,四川省成都市  610041
  • 收稿日期:2011-09-20 修回日期:2011-10-21 出版日期:2012-03-11
  • 通讯作者: 苏全生,成都体育学院运动医学系,四川省成都市 610041
  • 作者简介:付玉★,女,1985年生,湖北省利川市人,土家族,四川省成都体育学院在读硕士,主要从事运动性疲劳的机制与恢复研究。 flytogether0909@163.com
  • 基金资助:

    国家体育总局运动医学实验室重点资助项目(D210104)。

Influence of exercise on mitochondrial biological characteristics and cell senescence 

Fu Yu, Wang Wen-di, Xu Su-yang, Su Quan-sheng   

  1. Department of Sports Medicine, Chengdu Sport University, Chengdu  610041, Sichuan Province, China
  • Received:2011-09-20 Revised:2011-10-21 Online:2012-03-11
  • Contact: author: Su Quan-sheng, Department of Sports Medicine, Chengdu Sport University, Chengdu 610041, Sichuan Province, China
  • About author:Fu Yu★, Studying for master’s degree, Department of Sports Medicine, Chengdu Sport University, Chengdu 610041, Sichuan Province, China flytogether0909@163.com
  • Supported by:

    the Key Project of General Administration of Sport of China for Sports Medicine Laboratory, No. D210104*

摘要:

背景:线粒体结构和功能的改变与细胞衰老有密切联系。
目的:归纳线粒体生物学性状改变对细胞衰老的影响。
方法:应用计算机检索Medline数据库(1990-01/2011-06)、中国期刊全文数据库(1994-01/2011-06)、万方数据库(1994-01/2011-06)中有关线粒体对细胞衰老影响的文章。
结果与结论:从线粒体呼吸链逸出形成的活性氧导致线粒体膜通透性升高,线粒体跨膜电位降低,ATP合成减少。持续的活性氧氧化作用使线粒体DNA损伤增多,导致线粒体结构功能严重受损,促进细胞衰老甚至死亡。有氧训练可显著提高机体的有氧代谢水平,增进有氧工作能力,并提高机体线粒体基质酶及呼吸链酶活性,降低糖酵解酶活性,减少线粒体的氧化损伤,降低线粒体DNA缺失突变率,使线粒体产生适应性变化,提高氧化磷酸化功能。在训练中应合理安排运动间歇,避免大强度训练对细胞的持续损伤造成线粒体结构功能下降,从而对延缓细胞及机体衰老起一定的积极作用。
关键词:线粒体;运动;细胞衰老;活性氧;线粒体DNA突变   
doi:10.3969/j.issn.1673-8225.2012.11.038

关键词: 线粒体, 运动, 细胞衰老, 活性氧, 线粒体DNA突变 

Abstract:

BACKGROUND: Changes in mitochondrial structure and function are closely linked with cell senescence.
OBJECTIVE: To sum up the influence of changes in mitochondrial biological characteristics on cell senescence.
METHODS: A computer-based search of Medline database was performed for articles about the influence of mitochondria and exercise on cell senescence published from January 1990 to June 2011 and the related articles published from January 1994 to June 2011 were searched in China Journal Full-text Database and Wanfang database.
RESULTS AND CONCLUSION: Reactive oxygen species originated from the mitochondrial respiratory chain lead to increasing mitochondrial membrane permeability, reducing mitochondrial transmembrane potential and decreasing adenosine-triphosphate synthesis. Sustained oxidation of mitochondrial reactive oxygen species increases the mitochondrial DNA damage, leads to serious damage in mitochondrial structure and function, and then promotes cellular senescence or even death. Aerobic training can significantly improve the body aerobic metabolism level, increase aerobic capacity, improve the activities of body mitochondrial respiratory chain enzyme and matrix enzyme, reduce the glycolytic activity, mitochondrial oxidative damage and the rate of mitochondrial DNA deletion mutation. Therefore the mitochondrial adaptation and oxidative phosphorylation activity are improved. In training, reasonable arrangements of intermittent exercise should be considered as well as avoiding the cell damage of continuing decline in mitochondrial structure and function caused by high intensity training. It may play a positive role in delaying the cell aging and organism aging.

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