Higher DNA repair in mitochondria of long-lived species

Positive correlation between genomic DNA repair and longevity has been classically described (reviewed in [1]). However, this corresponded to repair of exogenous DNA damage estimated as unscheduled DNA synthesis in fibroblasts (mitotic cells) after in vitro exposure to UV radiation. Such a correlation makes sense because a higher protection from exogenous damage, like that inflicted by UV radiation, is necessary in order for the already superior longevity potential of slowly aging animals to be phenotypically expressed. Long-lived animals can reach many decades of age only if the many different causes of early death due to extrinsic mortality (including UV-induced DNA damage and skin cancer) are avoided. That comparison can also be strongly biased by the much lower need of excision repair for removal of UV-induced lesions in rodents than in humans due to their fur and nocturnal habits.