Mitochondrial DNA repair in aging and disease

被引：147

作者：

Druzhyna, Nadiya M. ^{[1
]}

Wilson, Glenn L. ^{[1
]}

LeDoux, Susan P. ^{[1
]}

机构：

[1] Univ S Alabama, Dept Cell Biol & Neurosci, Mobile, AL 36688 USA

来源：

MECHANISMS OF AGEING AND DEVELOPMENT | 2008年 / 129卷 / 7-8期

关键词：

mitochondria; base excision repair; neurodegeneration; aging; cancer;

D O I：

10.1016/j.mad.2008.03.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mitochondria are organelles which, according to the endosymbiosis theory, evolved from purpurbacteria approximately 1.5 billion years ago. One of the unique features of mitochondria is that they have their own genome. Mitochondria replicate and transcribe their DNA semiautonomously. Like nuclear DNA, mitochondrial DNA (mtDNA) is constantly exposed to DNA damaging agents. Regarding the repair of mtDNA, the prevailing concept for many years was that mtDNA molecules suffering an excess of damage would simply be degraded to be replaced by newly generated successors copied from undamaged genomes. However, evidence now clearly shows that mitochondria contain the machinery to repair the damage to their genomes caused by certain endogenous or exogenous damaging agents. The link between mtDNA damage and repair to aging, neurodegeneration, and carcinogenesis-associated processes is the subject of this review. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：383 / 390

页数：8

共 135 条

[1] Depletion of mtDNA: Syndromes and genes [J].

Alberio, Simona ;

Mineri, Rossana ;

Tiranti, Valeria ;

Zeviani, Massimo .

MITOCHONDRION, 2007, 7 (1-2) :6-12

[2] OXIDANTS, ANTIOXIDANTS, AND THE DEGENERATIVE DISEASES OF AGING [J].

AMES, BN ;

SHIGENAGA, MK ;

HAGEN, TM .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :7915-7922

[3] Mitochondrial metabolism of reactive oxygen species [J].

Andreyev, AI ;

Kushnareva, YE ;

Starkov, AA .

BIOCHEMISTRY-MOSCOW, 2005, 70 (02) :200-214

[4] Mitochondrial endogenous oxidative damage has been overestimated [J].

Anson, RM ;

Hudson, E ;

Bohr, VA .

FASEB JOURNAL, 2000, 14 (02) :355-360

[5] MITOCHONDRIAL MUTATIONS MAY INCREASE OXIDATIVE STRESS - IMPLICATIONS FOR CARCINOGENESIS AND AGING [J].

BANDY, B ;

DAVISON, AJ .

FREE RADICAL BIOLOGY AND MEDICINE, 1990, 8 (06) :523-539

[6] 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

[7] Aging in vertebrates, and the effect of caloric restriction: a mitochondrial free radical production-DNA damage mechanism? [J].

Barja, G .

BIOLOGICAL REVIEWS, 2004, 79 (02) :235-251

[8] Mitochondrial disorders. A diagnostic challenge in clinical chemistry [J].

Bauer, MF ;

Gempel, K ;

Hofmann, S ;

Jaksch, M ;

Philbrook, C ;

Gerbitz, KD .

CLINICAL CHEMISTRY AND LABORATORY MEDICINE, 1999, 37 (09) :855-876

[9] Mitochondrial DNA in aging and degenerative disease [J].

Berdanier, CD ;

Everts, HB .

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 2001, 475 (1-2) :169-184

[10] 'To repair or not to repair -: no longer a question':: repair of mitochondrial DNA shielding against age and cancer [J].

Berneburg, Mark ;

Kamenisch, York ;

Krutmann, Jean ;

Roecken, Martin .

EXPERIMENTAL DERMATOLOGY, 2006, 15 (12) :1005-1015

← 1 2 3 4 5 6 7 8 9 10 →