Hormonal
Mitochondrial DNA (mtDNA) mutations accumulate with age primarily due to replication errors rather than oxidative damage, and while high levels of mutations can cause premature ageing, normal levels may not be the primary driver of ageing.
Focus on maintaining overall cellular health rather than targeting 'mitochondrial damage' specifically with antioxidants. The accumulation of mtDNA mutations is likely due to replication errors, not just oxidative stress. Strategies that support stem cell function and stress response (like exercise) may be more effective than trying to 'repair' mtDNA directly.
evidence from an increasing number of experimental studies has suggested that mtDNA mutations may be generated by replication errors rather than by accumulated oxidative damage.
Why this rating
Based on deep sequencing studies and comparison of mutator vs. deletor mouse models.
Source
The role of mitochondrial <scp>DNA</scp> mutations and free radicals in disease and ageing
Marie Lagouge et al. · Journal of Internal Medicine · 2013
DOI 10.1111/joim.12055
More from this paper
- Modulating reactive oxygen species (ROS) levels through antioxidant interventions does not consistently extend lifespan or delay age-related diseases, contradicting the mitochondrial free radical theory of ageing.Good
- Reactive oxygen species (ROS) function as essential signaling molecules that mediate stress responses and adaptation, rather than solely as damaging agents, a concept known as the 'gradual ROS response hypothesis'.Good
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