Mitochondrial reactive oxygen species cause major oxidative mitochondrial DNA damages and repair pathways
| Autor: | Zhenqiu Huang, Yanmin Zhang, Yinnan Chen |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0106 biological sciences
Mitochondrial DNA Aging DNA Repair DNA repair Oxidative phosphorylation Mitochondrion medicine.disease_cause 01 natural sciences DNA Mitochondrial General Biochemistry Genetics and Molecular Biology medicine Humans chemistry.chemical_classification Cell Nucleus Reactive oxygen species General Medicine Base excision repair Cell biology Mitochondria Oxidative Stress Mitochondrial DNA repair chemistry General Agricultural and Biological Sciences Carcinogenesis Reactive Oxygen Species Oxidation-Reduction 010606 plant biology & botany DNA Damage Signal Transduction |
| Zdroj: | Journal of biosciences. 45 |
| ISSN: | 0973-7138 |
| Popis: | Mitochondria-derived reactive oxygen species (mROS) are produced at a variety of sites and affect the function of bio-molecules. The anti-oxidant system from both mitochondria and cytosol tightly coordinate to maintain the redox balance of cells and reduce damage from mROS. Mitochondrial DNA (mtDNA) are highly susceptible to mROS, and are easily oxidized to accumulate DNA modifications. Frequent oxidative damages in mtDNA have been associated with neurological degeneration, inflammasomes, tumorigenesis, and malignant progression. Among mitochondrial DNA repair pathways, the base excision repair pathway has been extensively characterized to remove some of oxidative damages in mtDNA as efficiently as the nuclear base excision repair. The implications of other pathways remain unclear. This review focuses on: (i) Sources of mROS and the antioxidant system to balance redox status; (ii) major mtDNA lesions or damages from mROS-mediated oxidation and the reported repair pathways or repairing factors; (iii) cellular response of oxidized mtDNA and methods to identify oxidatively generated DNA modifications in pathological conditions. DNA damages caused by mROS have been increasingly implicated in diseases and aging, and thus we critically discuss methods of the oxidative modifications evaluation and the complexity of non-canonical DNA repair pathways in mitochondria. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink