Gene hypermethylation in blood leukocytes in humans long term after radiation exposure – Validation set

Кузьмина, Н. С.; Lapteva, N. Sh.; Rusinova, Galina; Azizova, Tamara V.; Vyazovskaya, N. S.; Рубанович, А. В.

doi:10.1016/j.envpol.2017.12.039

Cited by 12 publications

(5 citation statements)

References 31 publications

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“…The respective stem cells can then be activated and multiplied by clonal expansion when the organism reencounters the toxicant or other stimulus [ 71 ]. This process perfectly fits the explanation of some previously published retrospective data, e.g., differences in the DNA methylation pattern related to the length of full breastfeeding observed in children aged 7–15 years; or rapid manifestation of adaptation processes related to DNA methylation changes in former smokers; or persistent changes of CpG islands in gene promoters of blood cells detectable in humans exposed to ionizing radiation long time ago (2–46 years) [ 48 , 63 , 72 ].…”

Section: Epigenetic Aspects Of Human Adaptation To Environmental Psupporting

confidence: 88%

The Molecular Mechanisms of Adaptive Response Related to Environmental Stress

Rössnerová

Izzotti

Pulliero

et al. 2020

IJMS

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The exposure of living organisms to environmental stress triggers defensive responses resulting in the activation of protective processes. Whenever the exposure occurs at low doses, defensive effects overwhelm the adverse effects of the exposure; this adaptive situation is referred to as “hormesis”. Environmental, physical, and nutritional hormetins lead to the stimulation and strengthening of the maintenance and repair systems in cells and tissues. Exercise, heat, and irradiation are examples of physical hormetins, which activate heat shock-, DNA repair-, and anti-oxidative-stress responses. The health promoting effect of many bio-actives in fruits and vegetables can be seen as the effect of mildly toxic compounds triggering this adaptive stimulus. Numerous studies indicate that living organisms possess the ability to adapt to adverse environmental conditions, as exemplified by the fact that DNA damage and gene expression profiling in populations living in the environment with high levels of air pollution do not correspond to the concentrations of pollutants. The molecular mechanisms of the hormetic response include modulation of (a) transcription factor Nrf2 activating the synthesis of glutathione and the subsequent protection of the cell; (b) DNA methylation; and (c) microRNA. These findings provide evidence that hormesis is a toxicological event, occurring at low exposure doses to environmental stressors, having the benefit for the maintenance of a healthy status.

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Section: Epigenetic Aspects Of Human Adaptation To Environmental Psupporting

confidence: 88%

The Molecular Mechanisms of Adaptive Response Related to Environmental Stress

Rössnerová

Izzotti

Pulliero

et al. 2020

IJMS

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“…Furthermore, radiation treatment was found to recruit SP1 transcription factor in meningioma cells [42]. We also detected promoter hypermethylation of the glutathione metabolism gene GSTP1 in the irradiated cells which is in agreement with a previous study on irradiated leukocytes [43]. The alterations that we identified in these genes could potentially confer adaptation to radio-induced stress.…”

Section: Discussionsupporting

confidence: 91%

Accumulation of DNA methylation alterations in paediatric glioma stem cells following fractionated dose irradiation

et al. 2020

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Background: Radiation is an important therapeutic tool. However, radiotherapy has the potential to promote coevolution of genetic and epigenetic changes that can drive tumour heterogeneity, formation of radioresistant cells and tumour relapse. There is a clinical need for a better understanding of DNA methylation alterations that may follow radiotherapy to be able to prevent the development of radiation-resistant cells. Methods:We examined radiation-induced changes in DNA methylation profiles of paediatric glioma stem cells (GSCs) in vitro. Five GSC cultures were irradiated in vitro with repeated doses of 2 or 4 Gy. Radiation was given in 3 or 15 fractions. DNA methylation profiling using Illumina DNA methylation arrays was performed at 14 days postradiation. The cellular characteristics were studied in parallel. Results: Few fractions of radiation did not result in significant accumulation of DNA methylation alterations. However, extended dose fractionations changed DNA methylation profiles and induced thousands of differentially methylated positions, specifically in enhancer regions, sites involved in alternative splicing and in repetitive regions. Radiation induced dose-dependent morphological and proliferative alterations of the cells as a consequence of the radiation exposure.Conclusions: DNA methylation alterations of sites with regulatory functions in proliferation and differentiation were identified, which may reflect cellular response to radiation stress through epigenetic reprogramming and differentiation cues.

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“…They observed that GSTP1 and p16 hypermethylation were correlated with exposure. Expanding on their work in relation to the long-term effects of radiation exposure, Kuzmina et al ( 88 ) performed a validation study in a separate cohort of 49 workers from another nuclear plant. They again reported associations with methylation of the GSTP1 and p16 genes, and they additionally observed hypermethylation of the TP53 and SOD3 gene promoters in comparison to non-exposed individuals.…”

Section: Resultsmentioning

confidence: 99%

Toxicomethylomics revisited: A state-of-the-science review about DNA methylation modifications in blood cells from workers exposed to toxic agents

Jiménez-Garza

Ghosh

Barrow

et al. 2023

Front. Public Health

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IntroductionEpigenetic marks have been proposed as early changes, at the subcellular level, in disease development. To find more specific biomarkers of effect in occupational exposures to toxicants, DNA methylation studies in peripheral blood cells have been performed. The goal of this review is to summarize and contrast findings about DNA methylation in blood cells from workers exposed to toxicants.MethodsA literature search was performed using PubMed and Web of Science. After first screening, we discarded all studies performed in vitro and in experimental animals, as well as those performed in other cell types other than peripheral blood cells. Results: 116 original research papers met the established criteria, published from 2007 to 2022. The most frequent investigated exposures/labor group were for benzene (18.9%) polycyclic aromatic hydrocarbons (15.5%), particulate matter (10.3%), lead (8.6%), pesticides (7.7%), radiation (4.3%), volatile organic compound mixtures (4.3%), welding fumes (3.4%) chromium (2.5%), toluene (2.5%), firefighters (2.5%), coal (1.7%), hairdressers (1.7%), nanoparticles (1.7%), vinyl chloride (1.7%), and others. Few longitudinal studies have been performed, as well as few of them have explored mitochondrial DNA methylation. Methylation platforms have evolved from analysis in repetitive elements (global methylation), gene-specific promoter methylation, to epigenome-wide studies. The most reported observations were global hypomethylation as well as promoter hypermethylation in exposed groups compared to controls, while methylation at DNA repair/oncogenes genes were the most studied; studies from genome-wide studies detect differentially methylated regions, which could be either hypo or hypermethylated.DiscussionSome evidence from longitudinal studies suggest that modifications observed in cross-sectional designs may be transitory; then, we cannot say that DNA methylation changes are predictive of disease development due to those exposures.ConclusionDue to the heterogeneity in the genes studied, and scarcity of longitudinal studies, we are far away from considering DNA methylation changes as biomarkers of effect in occupational exposures, and nor can we establish a clear functional or pathological correlate for those epigenetic modifications associated with the studied exposures.

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Gene hypermethylation in blood leukocytes in humans long term after radiation exposure – Validation set

Cited by 12 publications

References 31 publications

The Molecular Mechanisms of Adaptive Response Related to Environmental Stress

The Molecular Mechanisms of Adaptive Response Related to Environmental Stress

Accumulation of DNA methylation alterations in paediatric glioma stem cells following fractionated dose irradiation

Toxicomethylomics revisited: A state-of-the-science review about DNA methylation modifications in blood cells from workers exposed to toxic agents

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