Mixed
Mitochondrial dysfunction, specifically the accumulation of somatic mtDNA mutations, causes premature aging phenotypes in mammals, whereas the associated increase in reactive oxygen species (ROS) is not the primary driver of this damage.
Focus on maintaining mitochondrial integrity through healthy lifestyle choices that support cellular repair mechanisms, rather than relying solely on antioxidant supplements to neutralize ROS. The accumulation of genetic errors in mitochondria over time is a key driver of aging, and current evidence suggests this is distinct from simple oxidative damage.
Studies of mtDNA mutator mice has shown that increased levels of somatic mtDNA mutations directly can cause a variety of ageing phenotypes... There is a tendency to automatically link mitochondrial dysfunction to increased generation of reactive oxygen species (ROS), however, is rather the experimental support for this concept weak. In fact, respiratory-chain-deficient mice... typically have minor or no increase of oxidative stress.
Why this rating
Strong experimental evidence from transgenic mouse models (mutator mice) showing direct causation of aging phenotypes, though human relevance is noted as 'remaining to be established'.
Source
Mitochondrial dysfunction as a cause of ageing
Aleksandra Trifunović et al. · Journal of Internal Medicine · 2008
DOI 10.1111/j.1365-2796.2007.01905.x
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