DNA damage and rpair with age in individual human lymphocytes
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Changes in DNA double-strand break repair during aging correlate with an increase in genomic mutations
2022, Journal of Molecular BiologyCitation Excerpt :At the same time however, the rate of DNA repair decreases. Indeed, cells from older individuals show a lower rate of DSB repair compared to cells from younger individuals32,51. However, identifying the molecular underpinnings that drive age-related increases in genome instability has remained a challenge.42
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2020, Journal of Trace Elements in Medicine and BiologyEffect of age and sex on the level of DNA strand breaks and oxidatively damaged DNA in human blood cells
2019, Mutation Research - Genetic Toxicology and Environmental MutagenesisCitation Excerpt :Instead other predictors such as plasma lipids, HbA1c and alcohol consumption remained statistically significant, indicating the age-dependent effect on levels of Fpg-sensitive sites was mediated by these lifestyle factors. The studies on age-differences in levels of DNA strand breaks have shown positive [10,17–27], equivocal [14,15], null [9,11,12,16,28–32], or negative association [33]. Table 1 outlines a segregation of the studies into groups, based on the overall conclusion of the results and inclusion of adjustment and age scale (categorical or linear) in the statistical analysis.
Caliphruria subedentata (Amaryllidaceae) decreases genotoxicity and cell death induced by β-amyloid peptide in SH-SY5Y cell line
2018, Mutation Research - Genetic Toxicology and Environmental MutagenesisDNA double strand break repair, aging and the chromatin connection
2016, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisCitation Excerpt :Several studies showed reduced levels of DSB repair enzymes in aged tissues [13,14] and senescent cells [15,16]. Direct measurements of DNA repair functions in cells of young and old individuals showed that DSB repair declines in peripheral lymphocytes of aged human donors [17–19]; DSB repair by nonhomologous end joining (NHEJ) declines in multiple tissues of aged mice [20], rats [21,22], and both NHEJ [23] and homologous recombination (HR) pathways decline in replicatively senescent cells [16]. Other strong evidence for the importance of DSB repair to aging comes from the fact that mutations in multiple genes involved in DSB repair lead to premature aging phenotypes.
The comet assay: Reflections on its development, evolution and applications
2016, Mutation Research - Reviews in Mutation ResearchCitation Excerpt :Thus began our collaboration. We exchanged phone calls and letters, and over the next ten years we would publish several papers [11–17], beginning with the 1988 paper that forms the basis of what is now known as the comet assay. In 1985, for several months after my appointment at OSU ended, I was jobless and I spent the time thinking of the ideal technique to assess DNA damage.