Genetic polymorphisms in XRCC1, OGG1, APE1 and XRCC3 DNA repair genes, ionizing radiation exposure and chromosomal DNA damage in interventional cardiologists

Andreassi, Maria Grazia; Foffa, Ilenia; Manfredi, Samantha; Botto, Nicoletta; Cioppa, Angelo; Picaño, Eugenio

doi:10.1016/j.mrfmmm.2009.04.003

Cited by 65 publications

(35 citation statements)

References 44 publications

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“…Although the mechanism of these phenomena is complex, the production of ROS triggered by ionizing radiation appears to play a central role. ROS may damage cell structures and, most importantly, DNA 27–29 as well as result in pathological health effects including inflammation, fibrosis, necrosis 1 and cancer 13–15 . Chronic exposure to low doses of radiation may lead to systemic oxidative stress, as suggested by the increased level of MDA and circulating O 2 •− in high-dose radiologic procedures (i.e.…”

Section: Discussionmentioning

confidence: 99%

Redox status in workers occupationally exposed to long-term low levels of ionizing radiation: A pilot study

et al. 2016

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Objectives Reactive oxygen species (ROS), including superoxide (O2•−), play an important role in the biological effects of ionizing radiation. The human body has developed different antioxidant systems to defend against excessive levels of ROS. The aim of the present study is to investigate the redox status changes in the blood of radiologic technologists and compare these changes to control individuals. Methods We enrolled 60 medical workers: 20 occupationally exposed to ionizing radiation (all radiologic technologists), divided in three subgroups: conventional radiography (CR), computerized tomography (CT) and interventional radiography (IR) and 40 age- and gender-matched unexposed controls. Levels of O2•− and malondialdehyde (MDA) in blood were measured as an index of redox status, as were the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase. Redox status was also assessed by measuring levels of reduced and oxidized glutathione (GSH, GSSG, respectively). Results Levels of O2•− and MDA, and SOD activity in the blood of IR and CT-exposed subjects were significantly higher than both the CR-exposed subjects and control individuals. However, there were no statistically significant differences in the levels of catalase, GSH and ratio of GSH/GSSG between exposed workers and control individuals. Discussion This study suggests that healthcare workers in CT and IR occupationally exposed to radiation have an elevated circulating redox status as compared to unexposed individuals.

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Section: Discussionmentioning

confidence: 99%

Redox status in workers occupationally exposed to long-term low levels of ionizing radiation: A pilot study

et al. 2016

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“…The DNA repair system consists of several distinct pathways, including the base excision repair (BER) pathway and double-strand break (DSB) repair process [5]. BER pathway is a DNA repair process which operates on small lesions such as oxidized or reduced bases, fragmented or non-bulky adducts, or those produced by methylating agents and still acting on bases deamination injury induced by environmental carcinogens or endogenous sources [1,2,6].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of DNA damage in COPD patients and its correlation with polymorphisms in repair genes

et al. 2013

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BackgroundWe investigated a potential link between genetic polymorphisms in genes XRCC1 (Arg399Gln), OGG1 (Ser326Cys), XRCC3 (Thr241Met), and XRCC4 (Ile401Thr) with the level of DNA damage and repair, accessed by comet and micronucleus test, in 51 COPD patients and 51 controls.MethodsPeripheral blood was used to perform the alkaline and neutral comet assay; and genetic polymorphisms by PCR/RFLP. To assess the susceptibility to exogenous DNA damage, the cells were treated with methyl methanesulphonate for 1-h or 3-h. After 3-h treatment the % residual damage was calculated assuming the value of 1-h treatment as 100%. The cytogenetic damage was evaluated by buccal micronucleus cytome assay (BMCyt).ResultsCOPD patients with the risk allele XRCC1 (Arg399Gln) and XRCC3 (Thr241Met) showed higher DNA damage by comet assay. The residual damage was higher for COPD with risk allele in the four genes. In COPD patients was showed negative correlation between BMCyt (binucleated, nuclear bud, condensed chromatin and karyorrhexic cells) with pulmonary function and some variant genotypes.ConclusionOur results suggest a possible association between variant genotypes in XRCC1 (Arg399Gln), OGG1 (Ser326Cys), XRCC3 (Thr241Met), and XRCC4 (Ile401Thr), DNA damage and progression of COPD.

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“…However, it causes damage to normal cells of living tissue vicinity to tumors, resulting in mutation, radiation sickness, cancer, and ultimately death [183, 184]. Several reports demonstrated that IR induced APE1 polymorphism through the analysis of blood in breast cancer patients or occupationally exposed workers [91–93]. In particular, diagnostic X-rays increase the risk of developmental abnormalities and cancer in the exposed individuals [185–187].…”

Section: Ape1 As a Prediction Marker Of Environmental Carcinogenesmentioning

confidence: 99%

Human AP Endonuclease 1: A Potential Marker for the Prediction of Environmental Carcinogenesis Risk

Park

Kim

et al. 2014

Oxidative Medicine and Cellular Longevity

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Human apurinic/apyrimidinic endonuclease 1 (APE1) functions mainly in DNA repair as an enzyme removing AP sites and in redox signaling as a coactivator of various transcription factors. Based on these multifunctions of APE1 within cells, numerous studies have reported that the alteration of APE1 could be a crucial factor in development of human diseases such as cancer and neurodegeneration. In fact, the study on the combination of an individual's genetic make-up with environmental factors (gene-environment interaction) is of great importance to understand the development of diseases, especially lethal diseases including cancer. Recent reports have suggested that the human carcinogenic risk following exposure to environmental toxicants is affected by APE1 alterations in terms of gene-environment interactions. In this review, we initially outline the critical APE1 functions in the various intracellular mechanisms including DNA repair and redox regulation and its roles in human diseases. Several findings demonstrate that the change in expression and activity as well as genetic variability of APE1 caused by environmental chemical (e.g., heavy metals and cigarette smoke) and physical carcinogens (ultraviolet and ionizing radiation) is likely associated with various cancers. These enable us to ultimately suggest APE1 as a vital marker for the prediction of environmental carcinogenesis risk.

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Genetic polymorphisms in XRCC1, OGG1, APE1 and XRCC3 DNA repair genes, ionizing radiation exposure and chromosomal DNA damage in interventional cardiologists

Cited by 65 publications

References 44 publications

Redox status in workers occupationally exposed to long-term low levels of ionizing radiation: A pilot study

Redox status in workers occupationally exposed to long-term low levels of ionizing radiation: A pilot study

Evaluation of DNA damage in COPD patients and its correlation with polymorphisms in repair genes

Human AP Endonuclease 1: A Potential Marker for the Prediction of Environmental Carcinogenesis Risk

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