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DNA damage accumulation and repair decline

In mice, the DNA repair process of non-homologous end-joining that repairs DNA double strand breaks, declines in efficiency from 1.8-3.8-fold, depending on the specific tissue, when 5 month old animals are compared to 24 month old animals. A study of fibroblast cells from humans varying in age from 16-75 years showed that the efficiency and fidelity of non-homologous end joining, and the efficiency of homologous recombinational DNA repair decline with age leading to increased sensitivity to ionizing radiation in older individuals. In middle aged human adults, oxidative DNA damage was found to be greater among individuals who were both frail and living in poverty.