How radiation-specific is the dicentric assay?

Hoffmann, Wolfgang; Schmitz-Feuerhake, Inge

doi:10.1038/sj.jea.7500008

Cited by 31 publications

(16 citation statements)

References 140 publications

(140 reference statements)

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“…This might point to the effects of radiation exposure. Dicentrics are considered to be specific biomarkers of damage caused by ionizing radiation (Lloyd et al, 1992;Hoffmann and Schmitz-Feuerhake, 1999;Rozgaj et al, 2002). Sex, age or smoking did not significantly contribute to the incidence of chromosome aberrations.…”

Section: Discussionmentioning

confidence: 99%

Chromosome damage in workers in cigarette manufacturing industry

Milić¹,

Kašuba²,

Oreščanin³

et al. 2008

J of Applied Toxicology

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To investigate whether occupational exposure to tobacco dust is genotoxic, a group of employees in a tobacco factory was tested for structural chromosome aberrations (CA), cytokinesis-block micronucleus assay (CBMN) and sister chromatid exchanges (SCE) that are well established as indicators of early biological effects. The study group consisted of 40 tobacco workers and an equal number of matched controls. The results obtained in the exposed group showed a significant increase in chromosome aberrations (R=0.26), micronucleus frequency (R=0.56) and in sister chromatid exchanges (R=0.75), which was additionally influenced by smoking. A significant increase in high frequency cells (HFC) in the exposed group was also observed. Like the SCE frequency, the HFC frequency increased significantly in smokers of the control and exposed smokers. The study indicates that occupational exposure to tobacco dust induces genome damage. A higher risk was observed in women. The micronucleus frequency and sister chromatid exchange tests seem to be more reliable indicators of genome damage than chromosome aberrations in monitoring chronically exposed subjects.

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Section: Discussionmentioning

confidence: 99%

Chromosome damage in workers in cigarette manufacturing industry

Milić¹,

Kašuba²,

Oreščanin³

et al. 2008

J of Applied Toxicology

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“…Translocations increased with the square of the age in both the control and irradiated groups. The quantification of dicentrics in cultured, peripheral lymphocytes at first mitosis is the preferred 'biological dosimeter' for radiation exposures [73]. Although there is inconsistency in the age-dependent trends for background dicentrics [74], some studies including that of Ramsey et al [75], show an increasing frequency of aberrations from the newborn to the very old.…”

Section: Comparison Of Aging and Radiation Effectsmentioning

confidence: 99%

Ionizing radiation and aging: rejuvenating an old idea

Richardson

2009

Aging

118

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This paper reviews the contemporary evidence that radiation can accelerate aging, degenerative health effects and mortality. Around the 1960s, the idea that ionizing radiation caused premature aging was dismissed as the radiation-induced health effects appeared to be virtually confined to neoplasms. More recently, radiation has become associated with a much wider spectrum of age-related diseases, including cardiovascular disease; although some diseases of old age, such as diabetes, are notably absent as a radiation risk. On the basis of recent research, is there a stronger case today to be made linking radiation and aging? Comparison is made between the now-known biological mechanisms of aging and those of radiation, including oxidative stress, chromosomal damage, apoptosis, stem cell exhaustion and inflammation. The association between radiation effects and the free-radical theory of aging as the causative hypothesis seems to be more compelling than that between radiation and the nutrient-sensing TOR pathway. Premature aging has been assessed by biomarkers in calorie restriction studies; yet, biomarkers such as telomere erosion and p16INK4a are ambiguous for radiation-induced aging. Some animal studies suggest low dose radiation may even demonstrate hormesis health benefits. Regardless, there is virtually no support for a life span extending hypothesis for A-bomb survivors and other exposed subjects.

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“…In fact, DNA damage-related changes such as phosphorylation of H2AX at Ser-139 (γ-H2AX) 1 and the dicentric chromosome assay 8 have been established as the most reliable signatures of radiation exposure. Radiation was shown to cause DNA damage by production of ROS such as hydroxyl radical or by direct cleavage of covalent bonds in DNA molecule 22–25 .…”

Section: Discussionmentioning

confidence: 99%

Metabolomics Reveals Aging-associated Attenuation of Noninvasive Radiation Biomarkers in Mice: Potential Role of Polyamine Catabolism and Incoherent DNA Damage-repair

et al. 2013

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Development of methods for rapid screening and stratification of subjects after exposure is an integral part of countermeasures against radiation. The potential demographic and exposure history-related heterogeneity of exposed populations warrants robust biomarkers that withstand and reflect such differences. In this study, the effect of aging and repeated exposure on the metabolic response to sub-lethal irradiation was examined in mice using UPLC-ESI-TOF mass spectrometry. Aging attenuated post-exposure elevation in excretions of DNA damage biomarkers as well as N1-acetylspermidine. Although N1-acetylspermidine and 2’-deoxyuridine elevation was highly correlated in all age groups, xanthine and N1-acetylspermidine elevation was poorly correlated in older mice. These results may reflect the established decline in DNA damage-repair efficiency associated with aging and indicate a novel role for polyamine metabolism in the process. Although repeated irradiation at long intervals did not affect the elevation of N1-acetylspermidine, 2’-deoxyuridine, and xanthine, it did significantly attenuate the elevation of 2’-deoxycytidine and thymidine compared to a single exposure. However, these biomarkers were found to identify exposed subjects with accuracy ranging from 82% (xanthosine) to 98% (2’-deoxyuridine), irrespective of their age and exposure history. This indicates that metabolic biomarkers can act as robust noninvasive signatures of sub-lethal radiation exposure.

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How radiation-specific is the dicentric assay?

Cited by 31 publications

References 140 publications

Chromosome damage in workers in cigarette manufacturing industry

Chromosome damage in workers in cigarette manufacturing industry

Ionizing radiation and aging: rejuvenating an old idea

Metabolomics Reveals Aging-associated Attenuation of Noninvasive Radiation Biomarkers in Mice: Potential Role of Polyamine Catabolism and Incoherent DNA Damage-repair

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