Cellular senescence and organismal aging are both accompanied by increased DNA damage. Furthermore, damaged DNA has been shown to accumulate during aging in many tissues, including brain, muscle, kidney and liver. It remains to be determined if DNA damage is purely a result of the aging process or part of the cause. Several studies have shown that dietary (calorie) restriction reduces the amount of age-associated oxidative DNA damage.
Eukaryotic and prokaryotic cells possess multiple mechanisms to repair DNA and control age-associated damage to their genomes. These include base excision repair (BER) and nucleotide excision repair (NER) that excise and replace damaged nucleotide bases and helix-distorting lesions, respectively. Many of the proteins involved in NER are also active in the related transcription-coupled repair (TCR). In addition, mismatch repair (MMR) proteins act to replace mismatched nucleotides and repair insertion/deletion loops. Furthermore, there are two types of double-stranded DNA break repair, homologous recombination (HR) and non-homologous end-joining (NHEJ).