Mitochondrial and Nuclear DNA Oxidative Damage in Physiological and Pathological Aging

被引:91
作者
Kowalska, Marta [1 ]
Piekut, Thomas [1 ]
Prendecki, Michal [1 ]
Sodel, Agnieszka [1 ]
Kozubski, Wojciech [2 ]
Dorszewska, Jolanta [1 ]
机构
[1] Poznan Univ Med Sci, Dept Neurol, Neurobiol Lab, 49 Przybyszewskiego St, PL-60355 Poznan, Poland
[2] Poznan Univ Med Sci, Chair & Dept Neurol, Poznan, Poland
关键词
mitochondria; ROS; oxidative damage; mtDNA; aging; Alzheimer's disease; Parkinson's disease; BASE EXCISION-REPAIR; MILD COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE BRAIN; GLYCOSYLASE; OGG1; PARKINSONS-DISEASE; COMPLEX-I; CALORIC RESTRICTION; GENE-TRANSCRIPTION; LIPID-PEROXIDATION; OXIDANT STRESS;
D O I
10.1089/dna.2019.5347
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondria play an important role in numerous processes, including energy generation, regulating ion homeostasis, and cell signaling. Mitochondria are also the main source of reactive oxygen species (ROS). Due to the oxidative environment within mitochondria, the macromolecules therein, for example, mtDNA, proteins, and lipids are more susceptible to sustaining damage. During aging, mitochondrial functions decline, partly as a result of an accumulation of mtDNA mutations, decreased mtDNA copy number and protein expression, and a reduction in oxidative capacity. The aim of this study was to summarize the knowledge on DNA oxidative damage in aging and age-related neurodegenerative diseases. It has been hypothesized that various ROS may play an important role not only in physiological senescence but also in the development of neurodegenerative diseases, for example, Alzheimer's disease and Parkinson's disease. Thus, mitochondria seem to be a potential target of novel treatments for neurodegenerative diseases.
引用
收藏
页码:1410 / 1420
页数:11
相关论文
共 128 条
[61]  
International A.s.D., 2015, WORLD ALZHEIMER REPO, DOI DOI 10.1111/J.0963-7214.2004.00293.X
[62]   Levels of reduced and oxidized coenzymeQ-10 and 8-hydroxy-2′-deoxyguanosine in the cerebrospinal fluid of patients with living Parkinson's disease demonstrate that mitochondrial oxidative damage and/or oxidative DNA damage contributes to the neurodegenerative process [J].
Isobe, Chiaki ;
Abe, Takashi ;
Terayama, Yasuo .
NEUROSCIENCE LETTERS, 2010, 469 (01) :159-163
[63]   Markers of oxidant stress that are clinically relevant in aging and age-related disease [J].
Jacob, Kimberly D. ;
Noren Hooten, Nicole ;
Trzeciak, Andrzej R. ;
Evans, Michele K. .
MECHANISMS OF AGEING AND DEVELOPMENT, 2013, 134 (3-4) :139-157
[64]   Mitochondria in homeostasis of reactive oxygen species in cell, tissues, and organism [J].
Jezek, P ;
Hlavatá, L .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2005, 37 (12) :2478-2503
[65]   Regulatory mechanisms of RNA function: emerging roles of DNA repair enzymes [J].
Jobert, Laure ;
Nilsen, Hilde .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2014, 71 (13) :2451-2465
[66]  
Kang Han Chang, 2018, Biomater Res, V22, P34
[67]   Parkinson's disease brain mitochondrial complex I has oxidatively damaged subunits and is functionally impaired and misassembled [J].
Keeney, Paula M. ;
Xie, Jing ;
Capaldi, Roderick A. ;
Bennett, James P., Jr. .
JOURNAL OF NEUROSCIENCE, 2006, 26 (19) :5256-5264
[68]   Sirtuins, Cell Senescence, and Vascular Aging [J].
Kida, Yujiro ;
Goligorsky, Michael S. .
CANADIAN JOURNAL OF CARDIOLOGY, 2016, 32 (05) :634-641
[69]   A Remarkable Age-Related Increase in SIRT1 Protein Expression against Oxidative Stress in Elderly: SIRT1 Gene Variants and Longevity in Human [J].
Kilic, Ulkan ;
Gok, Ozlem ;
Erenberk, Ufuk ;
Dundaroz, Mehmet Rusen ;
Torun, Emel ;
Kucukardali, Yasar ;
Elibol-Can, Birsen ;
Uysal, Omer ;
Dundar, Tolga .
PLOS ONE, 2015, 10 (03)
[70]   Oxidative damage to RNA: mechanisms, consequences, and diseases [J].
Kong, Qiongman ;
Lin, Chien-liang Glenn .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2010, 67 (11) :1817-1829