Abstract
Ionizing radiation (IR) is a major source of cellular damage and the immediate cellular response to IR has been well characterized. But the long-term impact of IR on cell function and its relationship with aging are not known. Here, we examined the IR effects on telomere length and other biomarkers 50 to 68 years post-exposure (two time points per person) in survivors of the atomic bombing at Hiroshima during WWII. We found that telomere length of leukocytes was inversely correlated with the dose of IR (p=0.008), and this effect was primarily found in survivors who were exposed at younger ages; specifically those <12 years old (p=0.0004). Although a dose-related retardation of telomere shortening with age was observed in the cross-sectional data, longitudinal follow-up after 11 years did not show IR exposure-related alteration of the rate of telomere shortening with age. In addition, IR diminished the associations between telomere length and selected aging biomarkers that were observed in survivors with no dose. These included uric acid metabolism, cytokines, and blood T cell counts. These findings showed long-lasting detrimental effects of IR on telomere length of leukocytes in both dose- and age-at-exposure dependent manner, and on alterations of biomarkers with aging.
Highlights
Ionizing radiation (IR) causes a wide range of changes in DNA, lipid, and protein leading to profound injury of exposed cells and tissues [1, 2]
We found a significant trend of reduced telomere length with increased radiation exposure (p for trend = 0·08) (Figure 1B)
We found that younger survivors displayed a great radiation dose-dependent reduction of telomere lengths (p for trend = 0.0004) but we did not find such a difference in the older age group (Figure 1C)
Summary
Ionizing radiation (IR) causes a wide range of changes in DNA, lipid, and protein leading to profound injury of exposed cells and tissues [1, 2]. The degree of the cellular injuries depends on the dose of radiation, length of exposure, type of exposed cells/tissues, and age of subjects [3,4,5]. The immediate cellular response to IR is characterized by an appearance of γ-H2AX foci at the DNA damage sites along with the activation and localization of DNA repair and other cellular machineries www.impactjournals.com/oncotarget Characteristic No dose (
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