The great majority of mutations that are not neutral in their effect are deleterious to a cells survival. Thus, in a population of cells comprising a tissue with replicating cells, mutant cells will tend to be lost. However, infrequent mutations that provide a survival advantage will tend to clonally expand at the expense of neighboring cells in the tissue. This advantage to the cell is disadvantageous to the whole organism, because such mutant cells can give rise to cancer. Thus dna damages in frequently dividing cells, because they give rise to mutations, are a prominent cause of cancer. In contrast, dna damages in infrequently dividing cells are likely a prominent cause of aging.

Replication may also be blocked and/or the cell may die. Descriptions of reduced function, characteristic of aging and associated with accumulation of dna damage, are given later in this article. In contrast to dna damage, a last mutation is a change in the base sequence of the dna. A mutation cannot be recognized by enzymes once the base change is present in both dna strands, and thus a mutation cannot be repaired. At the cellular level, mutations can cause alterations in protein function and regulation. Mutations are replicated when the cell replicates. In a population of cells, mutant cells will increase or decrease in frequency according to the effects of the mutation on the ability of the cell to survive and reproduce. Although distinctly different from each other, dna damages and mutations are related because dna damages often cause errors of dna synthesis during replication or repair and these errors are a major source of mutation. Given these properties of dna damage and mutation, it can be seen that dna damages are a special problem in non-dividing or slowly dividing cells, where unrepaired damages will tend to accumulate over time. On the other hand, in rapidly dividing cells, unrepaired dna damages that do not kill the cell by blocking replication will tend to cause replication errors and thus mutation.

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4, human populations studies show that single-nucleotide polymorphisms in dna repair genes, causing up-regulation of their expression, correlate with increases in longevity. 5, lombard. Compiled a lengthy list of mouse mutational models with pathologic features of premature aging, all caused by different dna repair defects. 6, freitas and de magalhães presented a comprehensive review and appraisal of the soorten dna damage theory of aging, including a detailed analysis of many forms of evidence linking dna damage to aging. As an example, they described a study showing that centenarians of 100 to 107 years of age had higher levels of two dna repair enzymes, parp1 and, ku70, than general-population old individuals of 69 to 75 years of age. 7 2, their analysis supported the hypothesis that improved dna repair leads to longer life span. Overall, they concluded that while the complexity of responses to dna damage remains only partly borstbeen understood, the idea that dna damage accumulation with age is the primary cause of aging remains an intuitive and powerful one. 2, in humans and other mammals, dna damage occurs frequently and. Dna repair processes have evolved to compensate. Citation needed, in estimates made for mice, dna lesions occur on average 25 to 115 times per minute in each cell, or about 36,000 to 160,000 per cell per day. 8, some dna damage may remain in any cell despite the action of repair processes.

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Hypothesis that aging is caused by accumulated dna damage. The, dNA damage theory of aging proposes that aging is a consequence of unrepaired accumulation of naturally occurring dna damages. Damage in this context is a dna alteration that has an abnormal structure. Although both mitochondrial and nuclear, dNA damage can contribute to aging, nuclear dna is the main subject of this analysis. Nuclear dna damage can contribute to aging either indirectly (by increasing apoptosis or cellular senescence ) or directly (by increasing cell dysfunction). 1 2 3, several review articles have shown that deficient dna repair, allowing greater accumulation of dna damages, causes premature aging; and that increased dna repair facilitates greater longevity. Mouse models of nucleotide-excisionrepair syndromes reveal a striking correlation between the degree to which specific dna repair pathways are compromised and the severity of accelerated aging, strongly suggesting a causal relationship.

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