The flux of free radical attack through mitochondrial DNA is related to aging rate.

Aging is a progressive and universal process originated endogenously which manifests best in post-mitotic cells. Available data indicate that the relation between oxidative stress and aging is due to the presence of low rates of mitochondrial free radical production and low degrees of fatty acid unsaturation of cellular membranes in the post-mitotic tissues of long-lived animals in relation to those of short-lived ones. Recent research shows that long-lived animals also have lower steady-state levels of oxidative damage in the mitochondrial DNA (mtDNA) of post-mitotic cells than short-lived species. This study shows that the flux of free radical attack to mtDNA is higher in short- than in long-lived animals, and proposes that this is a main determinant of the rate of accumulation of mtDNA mutations, and thus the rate of aging. This implies that aging has been slowed evolutionarily by mechanisms that decrease the generation of endogenous damage rather than try to intercept damaging agents, or to repair the damage already inflicted. The first kind of mechanisms are more efficient and less energetically expensive. Free radicals of mitochondrial origin, oxidative damage to DNA, evolution of aging rate, and possibilities and consequences of their future modification are also discussed.