ArticleJournal of the American Aging Association2000
Mitochondria, oxidative DNA damage, and aging.
Article in Journal of the American Aging Association, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Lactoferrin Ameliorates Dry Eye Disease Potentially through Enhancement of Short-Chain Fatty Acid Production by Gut Microbiota in Mice.International journal of molecular sciences · 2021Article
- Dysregulation of the Acrosome Formation Network by 8-oxoguanine (8-oxoG) in Infertile Sperm: A Case Report with Advanced Techniques.International journal of molecular sciences · 2021Article
- Traumatic brain injury-induced cerebral microbleeds in the elderly.GeroScience · 2021Review
- MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle-aged men.European journal of applied physiology · 2020Article
- Adenosine A2A receptor (A2AR) stimulation enhances mitochondrial metabolism and mitigates reactive oxygen species-mediated mitochondrial injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging.Aging · 2020Article
- 8-OxoG in GC-rich Sp1 binding sites enhances gene transcription in adipose tissue of juvenile mice.Scientific reports · 2019Article
- Antigenotoxic Effects of Biochaga and Dihydroquercetin (Taxifolin) on HOxidative medicine and cellular longevity · 2019Article
- Mitochondrial determinants of cancer health disparities.Seminars in cancer biology · 2017Review
- Aging asymmetry: systematic survey of changes in age-related biomarkers in the annual fish Nothobranchius guentheri.Fish physiology and biochemistry · 2017Article
- Loss of the antioxidant enzyme CuZnSOD (Sod1) mimics an age-related increase in absolute mitochondrial DNA copy number in the skeletal muscle.Age (Dordrecht, Netherlands) · 2016Article
- Mitochondrial structure and function are not different between nonfailing donor and end-stage failing human hearts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Natural Compounds Modulating Mitochondrial Functions.Evidence-based complementary and alternative medicine : eCAM · 2015Review
- Endogenous ROS levels in C. elegans under exogenous stress support revision of oxidative stress theory of life-history tradeoffs.BMC evolutionary biology · 2014Article
- Exploring the role of genetic variability and lifestyle in oxidative stress response for healthy aging and longevity.International journal of molecular sciences · 2013Review
- Within- and between-species study of extreme longevity--comments, commonalities, and goals.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protection from reactive oxygen species (ROS) and from mitochondrial oxidative damage is well known to be necessary to longevity. The relevance of mitochondrial DNA (mtDNA) to aging is suggested by the fact that the two most commonly measured forms of mtDNA damage, deletions and the oxidatively induced lesion 8-oxo-dG, increase with age. The rate of increase is species-specific and correlates with maximum lifespan. It is less clear that failure or inadequacies in the protection from reactive oxygen species (ROS) and from mitochondrial oxidative damage are sufficient to explain senescence. DNA containing 8-oxo-dG is repaired by mitochondria, and the high ratio of mitochondrial to nuclear levels of 8-oxo-dG previously reported are now suspected to be due to methodological difficulties. Furthermore, MnSOD -/+ mice incur higher than wild type levels of oxidative damage, but do not display an aging phenotype. Together, these findings suggest that oxidative damage to mitochondria is lower than previously thought, and that higher levels can be tolerated without physiological consequence. A great deal of work remains before it will be known whether mitochondrial oxidative damage is a "clock" which controls the rate of aging. The increased level of 8-oxo-dG seen with age in isolated mitochondria needs explanation. It could be that a subset of cells lose the ability to protect or repair mitochondria, resulting in their incurring disproportionate levels of damage. Such an uneven distribution could exceed the reserve capacity of these cells and have serious physiological consequences. Measurements of damage need to focus more on distribution, both within tissues and within cells. In addition, study must be given to the incidence and repair of other DNA lesions, and to the possibility that repair varies from species to species, tissue to tissue, and young to old.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.