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
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