Ageing and subcellular distribution of mitochondria: role of mitochondrial DNA deletions and energy production

被引:26
作者
Drew, B [1 ]
Leeuwenburgh, C [1 ]
机构
[1] Univ Florida, Biochem Aging Lab, Gainesville, FL 32611 USA
来源
ACTA PHYSIOLOGICA SCANDINAVICA | 2004年 / 182卷 / 04期
关键词
calorie restriction; intermyofibrillar mitochondria; metabolism; myofibres; subsarcolemmal mitochondria;
D O I
10.1111/j.1365-201X.2004.01371.x
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The rapid growing population of elderly illustrates the importance of understanding the mechanisms responsible for ageing and the detrimental effects on health associated with increasing age. One of the primary mechanisms may be because of the accumulation of mtDNA damage and oxidative damage with age. Previous studies have examined this correlation in post-mitotic tissues such as skeletal muscle, heart and brain with decreased mitochondrial function, such as enzymatic activities of the electron transport chain and ATP production. However, regional differences in the subcellular location of mitochondria exist and most studies have failed to differentiate the effects of these two autonomous fractions, the subsarcolemmal and intermyofibrillar populations. Hence, while future research attempts to explain the mechanisms responsible for ageing in the mitochondrion, it should also take into account the independent pathways of these two distinctly different populations.
引用
收藏
页码:333 / 341
页数:9
相关论文
共 76 条
[1]   Effects of aging on mitochondrial DNA copy number and cytochrome c oxidase gene expression in rat skeletal muscle, liver, and heart [J].
Barazzoni, R ;
Short, KR ;
Nair, KS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (05) :3343-3347
[2]   Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals [J].
Barja, G ;
Herrero, A .
FASEB JOURNAL, 2000, 14 (02) :312-318
[3]   Oxidative decay of DNA [J].
Beckman, KB ;
Ames, BN .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (32) :19633-19636
[4]   A MITOCHONDRIAL-DNA DELETION IN NORMALLY AGING AND IN ALZHEIMER BRAIN-TISSUE [J].
BLANCHARD, BJ ;
PARK, T ;
FRIPP, WJ ;
LERMAN, LS ;
INGRAM, VM .
NEUROREPORT, 1993, 4 (06) :799-802
[5]   MITOCHONDRIAL THEORY OF SENESCENCE - RESPIRATORY-CHAIN PROTEIN STUDIES IN HUMAN SKELETAL-MUSCLE [J].
BYRNE, E ;
TROUNCE, I ;
DENNETT, X .
MECHANISMS OF AGEING AND DEVELOPMENT, 1991, 60 (03) :295-302
[6]   Mitochondrial free radical generation, oxidative stress, and aging [J].
Cadenas, E ;
Davies, KJA .
FREE RADICAL BIOLOGY AND MEDICINE, 2000, 29 (3-4) :222-230
[7]   The T9176G mtDNA mutation severely affects ATP production and results in Leigh syndrome [J].
Carrozzo, R ;
Tessa, A ;
Vázquez-Memije, ME ;
Piemonte, F ;
Patrono, C ;
Malandrini, A ;
Dionisi-Vici, C ;
Vilarinho, L ;
Villanova, M ;
Schägger, H ;
Federico, A ;
Bertini, E ;
Santorelli, F .
NEUROLOGY, 2001, 56 (05) :687-690
[8]   MUSCLE METABOLISM DURING EXERCISE IN YOUNG AND OLDER UNTRAINED AND ENDURANCE-TRAINED MEN [J].
COGGAN, AR ;
ABDULJALIL, AM ;
SWANSON, SC ;
EARLE, MS ;
FARRIS, JW ;
MENDENHALL, LA ;
ROBITAILLE, PM .
JOURNAL OF APPLIED PHYSIOLOGY, 1993, 75 (05) :2125-2133
[9]   Oxidative capacity and ageing in human muscle [J].
Conley, KE ;
Jubrias, SA ;
Esselman, PC .
JOURNAL OF PHYSIOLOGY-LONDON, 2000, 526 (01) :203-210
[10]   INFLUENCE OF THE ENERGETIC PATTERN OF MITOCHONDRIA IN CELL AGING [J].
CORBISIER, P ;
REMACLE, J .
MECHANISMS OF AGEING AND DEVELOPMENT, 1993, 71 (1-2) :47-58