23 results on '"CEPPI, MARCELLO"'
Search Results
2. DNA damage in circulating leukocytes measured with the comet assay may predict the risk of death.
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Bonassi S, Ceppi M, Møller P, Azqueta A, Milić M, Neri M, Brunborg G, Godschalk R, Koppen G, Langie SAS, Teixeira JP, Bruzzone M, Da Silva J, Benedetti D, Cavallo D, Ursini CL, Giovannelli L, Moretti S, Riso P, Del Bo' C, Russo P, Dobrzyńska M, Goroshinskaya IA, Surikova EI, Staruchova M, Barančokova M, Volkovova K, Kažimirova A, Smolkova B, Laffon B, Valdiglesias V, Pastor S, Marcos R, Hernández A, Gajski G, Spremo-Potparević B, Živković L, Boutet-Robinet E, Perdry H, Lebailly P, Perez CL, Basaran N, Nemeth Z, Safar A, Dusinska M, and Collins A
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- Comet Assay, Humans, Kaplan-Meier Estimate, Leukocytes pathology, Neoplasms mortality, Proportional Hazards Models, Cell-Free Nucleic Acids genetics, DNA Damage genetics, Neoplasms genetics
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The comet assay or single cell gel electrophoresis, is the most common method used to measure strand breaks and a variety of other DNA lesions in human populations. To estimate the risk of overall mortality, mortality by cause, and cancer incidence associated to DNA damage, a cohort of 2,403 healthy individuals (25,978 person-years) screened in 16 laboratories using the comet assay between 1996 and 2016 was followed-up. Kaplan-Meier analysis indicated a worse overall survival in the medium and high tertile of DNA damage (p < 0.001). The effect of DNA damage on survival was modelled according to Cox proportional hazard regression model. The adjusted hazard ratio (HR) was 1.42 (1.06-1.90) for overall mortality, and 1.94 (1.04-3.59) for diseases of the circulatory system in subjects with the highest tertile of DNA damage. The findings of this study provide epidemiological evidence encouraging the implementation of the comet assay in preventive strategies for non-communicable diseases., (© 2021. The Author(s).)
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- 2021
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3. DNA damage and genomic instability among workers formerly and currently exposed to asbestos.
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Milić M, Neri M, Ceppi M, Bruzzone M, Munnia A, Ugolini D, Cristaudo A, Bonotti A, Peluso ME, and Bonassi S
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- Cross-Sectional Studies, European Union, Humans, Male, Micronucleus Tests methods, Middle Aged, Occupational Health, Risk Assessment, Surveys and Questionnaires, Asbestos adverse effects, DNA Damage genetics, Genomic Instability genetics, Occupational Exposure standards
- Abstract
Objectives Despite an asbestos ban in the European Union, exposure to asbestos still represents an occupational risk. Biomarkers of DNA damage and genomic instability in groups exposed to asbestos may contribute to the identification of subgroups/subjects at higher risk. Methods A cross-sectional study was conducted on 468 male individuals (80 working in occupational settings with potential exposure to asbestos fibers, 202 retired workers with past exposure, and 186 non-exposed controls) to compare genomic instability, cell proliferation and differentiation level using the non-invasive micronucleus buccal cytome assay. Data on demographic variables, lifestyle, and occupational history were collected with a standardized questionnaire. Micronuclei (MN) and other biomarkers of DNA damage and genomic instability were scored in a minimum of 2000/1000 cells per individual, respectively. Results Univariate and multivariate analysis showed opposite associations of MN frequency with current and former exposure. Compared to unexposed controls, workers with current potential exposure to asbestos had 55% lower MN frequency [95% confidence interval (CI) 71-29%, P<0.001] while those with past exposure had 34% higher MN frequency (95% CI 1-77%, P<0.001). The frequency of cells with condensed chromatin and binucleated cells was elevated among formerly exposed workers. The multivariate analysis did not reveal any actual confounders, although lower MN frequency was observed among subjects eating fresh fruit or vegetables every day or taking vitamin supplements. Conclusions Active workers with potential exposure to asbestos fibers did not show increased genomic damage. On the contrary, workers exposed in the past experienced a persistently elevated genomic instability, which may be used for risk assessment at subgroup or individual level.
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- 2018
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4. Clinical application of micronucleus test in exfoliated buccal cells: A systematic review and metanalysis.
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Bolognesi C, Bonassi S, Knasmueller S, Fenech M, Bruzzone M, Lando C, and Ceppi M
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- Humans, DNA Damage genetics, Micronucleus Tests methods, Mouth Mucosa cytology, Mouth Mucosa metabolism, Mouth Neoplasms diagnosis, Mouth Neoplasms genetics
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The micronucleus assay in uncultured exfoliated buccal mucosa cells, involving minimally invasive sampling, was successfully applied to evaluate inhalation and local exposure to genotoxic agents, impact of nutrition and lifestyle factors. The potential use of the assay in clinics to monitor the development of local oral lesions and as an early biomarker for tumors and different chronic disorders was also investigated. A systematic review of the literature was carried out focusing on the clinical application of the assay. The literature search updated to January 2015 allowed to retrieve 42 eligible articles. Fifty three percent of investigations are related to oral, head and neck cancer, and premalignant oral diseases. Our analysis evidences a potential usefulness of the MN assay applied in buccal exfoliated cells in the prescreening and in the follow up of precancerous oral lesions. A significant excess of MN, in patients compared with matched controls was observed for subgroups of oral and neck cancer (meta-MR of 2.40, 95% CI: 2.02-2.85) and leukoplakia (meta-MR 1.88, 95% CI: 1.51-2.35). The meta-analysis of studies available on other tumors (meta-MR 2.00; 95% CI:1.66-2.41) indicates that the MN frequency in buccal cells could reflect the chromosomal instability of other organs. Increased MN frequency was also observed in small size studies on patients with chronic diseases, with Alzheimer's disease and with Down syndrome. The application of the cytome approach providing information of genotoxic, cytotoxic and cytostatic effects is suggestive of the possibility of an improvement in the predictive value of the assay and this deserves further investigations., (Copyright © 2015 Elsevier B.V. All rights reserved.)
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- 2015
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5. Oxidatively damaged DNA in the nasal epithelium of workers occupationally exposed to silica dust in Tuscany region, Italy.
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Peluso ME, Munnia A, Giese RW, Chellini E, Ceppi M, and Capacci F
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- Adult, Cross-Sectional Studies, DNA Adducts drug effects, Female, Follow-Up Studies, Humans, Incidence, Italy epidemiology, Male, Middle Aged, Nasal Mucosa drug effects, Occupational Diseases chemically induced, Occupational Diseases pathology, Oxidation-Reduction, Prognosis, DNA Damage drug effects, Dust, Nasal Mucosa pathology, Occupational Diseases epidemiology, Occupational Exposure adverse effects, Oxidative Stress drug effects, Silicon Dioxide adverse effects
- Abstract
Unlabelled: Chronic silica exposure has been associated to cancer and silicosis. Furthermore, the induction of oxidative stress and the generation of reactive oxygen species have been indicated to play a main role in the carcinogenicity of respirable silica. Therefore, we conducted a cross-sectional study to evaluate the prevalence of 3-(2-deoxy-β-D-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M1dG) adducts, a biomarker of oxidative stress and peroxidation of lipids, in the nasal epithelium of 135 silica-exposed workers, employed in pottery, ceramic and marble manufacturing plants as well as in a stone quarry, in respect to 118 controls living in Tuscany region, Italy. The M1dG generation was measured by the (32)P-postlabelling assay. Significant higher levels of M1dG adducts per 10(8) normal nucleotides were observed in the nasal epithelium of smokers, 77.9±9.8 (SE), and in those of former smokers, 80.7±9.7 (SE), as compared to non-smokers, 57.1±6.2 (SE), P = 0.001 and P = 0.004, respectively. Significant increments of M1dG adducts were found in the nasal epithelium of workers that handle artificial marble conglomerates, 184±36.4 (SE), and in those of quarry workers, 120±34.7 (SE), with respect to controls, 50.6±2.7 (SE), P = 0.014 and P < 0.001, respectively. Null increments were observed in association with the pottery and the ceramic factories. After stratification for different exposures, silica-exposed workers that were co-exposed to organic solvents, and welding and exhaust fumes have significantly higher M1dG levels, 90.4±13.4 (SE), P = 0.014 vs., Control: Our data suggested that silica exposure might be associated with genotoxicity in the nasal epithelial cells of silica-exposed workers that handle of artificial marble conglomerates and quarry workers. Importantly, we observed that co-exposures to other respiratory carcinogens may have contributed to enhance the burden of M1dG adducts in the nasal epithelium of silica-exposed workers., (© The Author 2015. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
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- 2015
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6. DNA adducts and combinations of multiple lung cancer at-risk alleles in environmentally exposed and smoking subjects.
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Peluso ME, Munnia A, Srivatanakul P, Jedpiyawongse A, Sangrajrang S, Ceppi M, Godschalk RW, van Schooten FJ, and Boffetta P
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- DNA-(Apurinic or Apyrimidinic Site) Lyase genetics, Environmental Exposure, Epoxide Hydrolases genetics, Genetic Predisposition to Disease, Genetic Variation, Humans, NAD(P)H Dehydrogenase (Quinone) genetics, Risk, Superoxide Dismutase genetics, DNA Adducts, DNA Damage, Lung Neoplasms genetics, Smoking, Tobacco Smoke Pollution
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Interindividual variation in DNA adduct levels in individuals exposed to similar amounts of environmental carcinogens may be due to genetic variability. We analysed the influence of genes involved in determining/modifying DNA damage, including microsomal epoxide hydrolase1 (EPHX1) His139Arg, N-acetyl-transferase, NAD(P)H:quinone oxidoreductase1 (NQO1) Pro187Ser, manganese superoxide dismutase2 (MnSOD2) Val16Ala, and apurinic/apyrimidinic endonuclease1 (APE1) Asp148Glu polymorphisms in blood of 120 smokers. Subsequently, we examined the effects of the combinations of the variant alleles of EPHX, NQO1 and MnSOD2 together with the wild type allele of APE1 on DNA damage by calculating the "sum of at-risk alleles." We reviewed the studies examining the relationships of DNA adducts with at-risk alleles in environmentally exposed subjects. Our findings showed that smokers carrying the EPHX1-139Arg and the NQO1-187Ser variants were significantly more likely to have higher adduct levels. Null associations were found with the other variants. Nevertheless, DNA adduct levels in smokers with ≥5 at-risk alleles were significantly different from those with fewer than two alleles. A similar picture emerged from studies of DNA adducts and at-risk alleles in environmentally exposed and smoking subjects. Certain at-risk allele combinations may confer a greater likelihood of increased levels of adducts after environmental insults. The increase in DNA adduct levels in susceptible subjects exposed to environmental carcinogens may reflect changes in the mechanisms that protect cells from the accumulation of genetic damage. Alterations of the physiological processes designed to maintain homeostasis may reduce the individual "genotoxic tolerance" to environmental challenges and result in phenotypes characterized by high levels of DNA adducts., (© 2013 Wiley Periodicals, Inc.)
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- 2013
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7. Study design and statistical analysis of data in human population studies with the micronucleus assay.
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Ceppi M, Gallo F, and Bonassi S
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- Age Factors, Data Interpretation, Statistical, Female, Genetic Markers, Humans, Male, Micronucleus Tests, Mouth Mucosa drug effects, Mouth Mucosa ultrastructure, Sample Size, Sex Factors, Smoking epidemiology, Smoking genetics, DNA Damage, Genetic Predisposition to Disease epidemiology, Micronuclei, Chromosome-Defective, Research Design
- Abstract
The most common study design performed in population studies based on the micronucleus (MN) assay, is the cross-sectional study, which is largely performed to evaluate the DNA damaging effects of exposure to genotoxic agents in the workplace, in the environment, as well as from diet or lifestyle factors. Sample size is still a critical issue in the design of MN studies since most recent studies considering gene-environment interaction, often require a sample size of several hundred subjects, which is in many cases difficult to achieve. The control of confounding is another major threat to the validity of causal inference. The most popular confounders considered in population studies using MN are age, gender and smoking habit. Extensive attention is given to the assessment of effect modification, given the increasing inclusion of biomarkers of genetic susceptibility in the study design. Selected issues concerning the statistical treatment of data have been addressed in this mini-review, starting from data description, which is a critical step of statistical analysis, since it allows to detect possible errors in the dataset to be analysed and to check the validity of assumptions required for more complex analyses. Basic issues dealing with statistical analysis of biomarkers are extensively evaluated, including methods to explore the dose-response relationship among two continuous variables and inferential analysis. A critical approach to the use of parametric and non-parametric methods is presented, before addressing the issue of most suitable multivariate models to fit MN data. In the last decade, the quality of statistical analysis of MN data has certainly evolved, although even nowadays only a small number of studies apply the Poisson model, which is the most suitable method for the analysis of MN data.
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- 2011
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8. DNA damage in Pakistani agricultural workers exposed to mixture of pesticides.
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Bhalli JA, Ali T, Asi MR, Khalid ZM, Ceppi M, and Khan QM
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- Adult, Chromatography, High Pressure Liquid, Comet Assay, Humans, Male, Pakistan, Spectrophotometry, Ultraviolet, Agriculture, DNA Damage, Occupational Exposure
- Abstract
A cross-sectional study was designed to determine whether occupational exposure to a complex mixture of pesticides results in a significant increase of DNA damage in farmers chronically exposed to pesticides in open fields. Leukocytes from 47 agriculture workers exposed to pesticides and 50 controls were evaluated with comet assay. Workers recruitment was based on their exposure to pesticides during the spraying season on cotton crop. Serum from these individuals was also analyzed for pesticides presence using high performance liquid chromatography. Statistically significant difference (P < 0.001) in DNA damage of exposed individuals (mean +/- S.D 14.80 +/- 3.04 microm) was observed when compared with control group (6.54 +/- 1.73 microm) as studied on the basis of comet tail length. Smokers had significantly higher mean comet tail length than nonsmokers and ex-smokers in both workers (20.26 +/- 3.53 vs. 14.19 +/- 4.25, P < 0.001) and controls (7.86 +/- 1.09 vs. 5.80 +/- 1.59, P < 0.001), whereas age had a minimal effect on DNA damage (P < 0.05). The length of pesticide exposure is positively associated with DNA damage in exposed individuals (P < 0.001). Our study shows that chronic exposure to pesticides produces DNA damage in pesticide sprayers and suggests that this type of monitoring is recommended in preventive policies for pesticide sprayers.
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- 2009
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9. Children's exposure to environmental pollutants and biomarkers of genetic damage. II. Results of a comprehensive literature search and meta-analysis.
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Neri M, Ugolini D, Bonassi S, Fucic A, Holland N, Knudsen LE, Srám RJ, Ceppi M, Bocchini V, and Merlo DF
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- Adolescent, Adult, Carcinogens, Child, Child, Preschool, Comet Assay, DNA Adducts, Environmental Monitoring, Female, Humans, Hypoxanthine Phosphoribosyltransferase, Infant, Infant, Newborn, Male, Polycyclic Aromatic Hydrocarbons, Pregnancy, Sister Chromatid Exchange, Smoking, Biomarkers, Chromosome Aberrations, DNA Damage, Databases, Factual, Environmental Exposure, Environmental Pollutants
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The present review is based on findings from 178 publications retrieved through an extensive search of the MedLine/PubMed database for a 25 years time period (1980-2004) and 10 manually identified papers. Among the cytogenetic biomarkers that are frequently used in field studies, chromosome aberrations (CA) and micronuclei (MN) but not sister chromatid exchanges (SCE) were found consistently increased in children exposed to environmental pollutants. Meta-analysis of the studies reporting SCE in cord blood showed similar levels of SCE in exposed and in non-exposed newborns. Exposure to airborne pollutants, soil and drinking water contaminants, mostly increased CA and, to a lesser extent, MN levels in children. The effect of exposure to airborne urban pollutants was consistently reported by field studies measuring DNA, albumin and hemoglobin adducts. Prenatal (in utero) and postnatal exposure (environmental tobacco smoke, ETS) to tobacco smoke compounds were associated with increased frequencies of DNA and hemoglobin adducts and CA. The limited number of field studies measuring DNA fragmentation (Comet assay), hypoxanthine-guanine phosphoribosyltransferase (HPRT) and the glycophorinA (GPA) mutation frequency in environmentally exposed children precluded a meaningful evaluation of the usefulness of these assays. Meta-analyses performed in children exposed to ETS and in newborns exposed in utero to their mothers' smoke showed 1.3 and 7 times higher levels of hemoglobin adducts compared to referent subjects, respectively. These increases are consistent with the epidemiological evidence of higher lung cancer risks reported in adults who had never smoked and were exposed to ETS during childhood and with 7-15 times higher lung cancer risks reported in smokers than in non-smokers. Higher levels of PAH-DNA adducts were found in fetal than in maternal tissue, suggesting a specific susceptibility of the fetus to this class of ubiquitous environmental pollutants. According to these findings, future research and biomonitoring programs on children would greatly benefit from the inclusion of selected biomarkers that could provide biologically based evidence for the identification of intervention priorities in environmental health.
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- 2006
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10. Effect of Air Pollution on the Basal DNA Damage of Mother–Newborn Couples of México City.
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Valverde, Mahara, Granados, Adriana, Milić, Mirta, Ceppi, Marcello, Sollano, Leticia, Bonassi, Stefano, and Rojas, Emilio
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AIR pollution ,DNA damage ,BIRTH weight ,LOW birth weight ,MATERNAL age ,PREGNANCY complications ,ENVIRONMENTAL exposure - Abstract
Environmental pollution of megacities can cause early biological damage such as DNA strand breaks and micronuclei formation. Comet assay tail length (TL) reflects exposure in the uterus to high levels of air pollution, primarily ozone and air particles (PM
10 ), including mothers' smoking habits during pregnancy, conditions which can lead to low birth weight. In this biomonitoring study, we evaluated basal DNA damage in the cord blood cells of newborn children from Mexico City. We found a correlation between DNA damage in mothers and their newborns, including various parameters of environmental exposure and complications during pregnancy, particularly respiratory difficulties, malformations, obstetric trauma, neuropathies, and nutritional deficiencies. Mothers living in the southern part of the city showed double DNA damage compared to those living in the northern part (TL 8.64 μm vs. 4.18 μm, p < 0.05). Additionally, mothers' DNA damage correlates with exposure to NOx (range 0.77–1.52 ppm) and PM10 (range 58.32–75.89 μg/m3 ), as well maternal age >29. These results highlight the sensitivity of the comet assay in identifying differential in utero exposure for newborns whose mothers were exposed during pregnancy. They also suggest the importance of antioxidants during pregnancy and the role of the placental barrier in protecting the newborn from the DNA-damaging effects of oxidative pollution. [ABSTRACT FROM AUTHOR]- Published
- 2023
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11. Malondialdehyde-Deoxyguanosine Adducts among Workers of a Thai Industrial Estate and Nearby Residents
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Peluso, Marco, Srivatanakul, Petcharin, Munnia, Armelle, Jedpiyawongse, Adisorn, Ceppi, Marcello, Sangrajrang, Suleeporn, Piro, Sara, and Boffetta, Paolo
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- 2010
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12. DNA damage in circulating leukocytes measured with the comet assay may predict the risk of death
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Bonassi, Stefano, Ceppi, Marcello, Møller, Peter, Azqueta, Amaya, Milić, Mirta, Monica, Neri, Brunborg, Gunnar, Godschalk, Roger, Koppen, Gudrun, Langie, Sabine A. S., Teixeira, João Paulo, Bruzzone, Marco, Da Silva, Juliana, Benedetti, Danieli, Cavallo, Delia, Ursini, Cinzia Lucia, Giovannelli, Lisa, Moretti, Silvia, Riso, Patrizia, Del Bo’, Cristian, Russo, Patrizia, Dobrzyńska, Malgorzata, Goroshinskaya, Irina A., Surikova, Ekaterina I., Staruchova, Marta, Barančokova, Magdalena, Volkovova, Katarina, Kažimirova, Alena, Smolkova, Bozena, Laffon, Blanca, Valdiglesias, Vanessa, Pastor, Susana, Marcos, Ricard, Hernández, Alba, Gajski, Goran, Spremo-Potparević, Biljana, Živković, Lada, Boutet-Robinet, Elisa, Perdry, Hervé, Lebailly, Pierre, Perez, Carlos L., Basaran, Nursen, Nemeth, Zsuzsanna, Safar, Anna, Dusinska, Maria, Collins, Andrew, Anderson, Diana, Andrade, Vanessa, Pereira, Cristiana Costa, Costa, Solange, Gutzkow, Kristine B., Ladeira, Carina, Moretti, Massimo, Costa, Carla, Orlow, Irene, Rojas, Emilio, Pourrut, Bertrand, Kruszewski, Marcin, Knasmueller, Siegfried, Shaposhnikov, Sergey, Žegura, Bojana, Stopper, Helga, LESUR, Hélène, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS San Raffaele Pisana), Ospedale Policlinico San Martino [Genoa], University of Copenhagen = Københavns Universitet (UCPH), Universidad de Navarra [Pamplona] (UNAV), Instituto de Investigación Sanitaria de Navarra [Pamplona, Spain] (IdiSNA), Institute for Medical Research and Occupational Health, Norwegian Institute of Public Health [Oslo] (NIPH), School of Nutrition and Translational Research in Metabolism [Maastricht] (NUTRIM), Maastricht University [Maastricht], Flemish Institute for Technological Research (VITO), Instituto Nacional de Saùde Dr Ricardo Jorge [Portugal] (INSA), Universidade Luterana do Brasil - ULBRA (BRAZIL), Universidade Luterana do Brasil (ULBRA), Istituto Nazionale per l’Assicurazione contro gli Infortuni sul Lavoro [Italian Workers Compensation Authority] (INAIL), NEUROFARBA Department [Firenze, Italy], Università degli Studi di Firenze = University of Florence (UniFI), Université de Florence, Università degli Studi di Milano = University of Milan (UNIMI), IRCCS San Raffaele Scientific Institute [Milan, Italie], National Institute of Public Health - National Institute of Hygiene [Poland], N.N. Blokhin National Medical Research Center of Oncology, Slovak Medical University of Bratislava (SMU), Slovak Academy of Science [Bratislava] (SAS), University of A Coruña (UDC), Instituto de Investigación Biomédica de A Coruña [La Corogne, Espagne] (INIBIC), A Coruña University Hospital [La Corogne, Espagne], Universitat Autònoma de Barcelona (UAB), CIBER de Epidemiología y Salud Pública (CIBERESP), School of Medecine [Belgrade], University of Belgrade [Belgrade], Contaminants & Stress Cellulaire (ToxAlim-COMICS), ToxAlim (ToxAlim), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Unité de recherche interdisciplinaire pour la prévention et le traitement des cancers (ANTICIPE), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Tumorothèque de Caen Basse-Normandie (TCBN)-Centre Régional de Lutte contre le Cancer François Baclesse [Caen] (UNICANCER/CRLC), Normandie Université (NU)-UNICANCER-Tumorothèque de Caen Basse-Normandie (TCBN)-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM), Instituto de Ciencias Básicas y Preclínicas Victoria de Girón, Hacettepe University = Hacettepe Üniversitesi, National center for public health [Hungary], Norwegian Institute for Air Research (NILU), University of Oslo (UiO), This article is based upon work from COST Action CA15132 (hCOMET), supported by COST (European Cooperation in Science and Technology). The work of SB and PR was supported by funds granted by the Italian Ministry of Health for Institutional Research (Ricerca Corrente)., Farmacologie en Toxicologie, RS: NUTRIM - R3 - Respiratory & Age-related Health, University of Copenhagen = Københavns Universitet (KU), Università degli Studi di Firenze = University of Florence [Firenze] (UNIFI), Università degli Studi di Milano [Milano] (UNIMI), CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN)-Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Régional de Lutte contre le Cancer François Baclesse [Caen] (UNICANCER/CRLC), UNICANCER-Tumorothèque de Caen Basse-Normandie (TCBN)-Normandie Université (NU)-UNICANCER, and Instituto de Saúde Pública da Universidade do Porto
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Oncology ,[SDV]Life Sciences [q-bio] ,Chromosomal aberrations ,Human cancer ,Lymphocytes ,Predicts ,Frequency ,Validation ,Biomarkers ,Hallmarks ,Adducts ,Repair ,Cohort ,Kaplan-Meier Estimate ,0302 clinical medicine ,Neoplasms ,Leukocytes ,Medicine ,Gel electrophoresis ,0303 health sciences ,Multidisciplinary ,Hazard ratio ,3. Good health ,[SDV] Life Sciences [q-bio] ,030220 oncology & carcinogenesis ,Biomarker (medicine) ,LYMPHOCYTES PREDICTS ,Comet Assay ,Cell-Free Nucleic Acids ,medicine.medical_specialty ,DNA damage ,Science ,FREQUENCY ,Article ,VALIDATION ,03 medical and health sciences ,ADDUCTS ,Internal medicine ,Humans ,COHORT ,Risk factor ,Author Correction ,030304 developmental biology ,Proportional Hazards Models ,HALLMARKS ,REPAIR ,HUMAN CANCER ,business.industry ,Proportional hazards model ,Comet assay, biomarker, leukocytes, epidemiology ,Comet assay ,CHROMOSOMAL-ABERRATIONS ,Risk factors ,Genotoxicidade Ambiental ,business ,DNA Damage - Abstract
Author Correction: https://doi.org/10.1038/s41598-021-98620-6. The original version of this Article contained errors: The spelling of the author Monica Neri was incorrectly given as Neri Monica; Additionally, Affiliation 39 was incorrectly given as ‘National Institute of Health, Lisbon, Portugal’, the correct affiliation is listed below: National Institute of Health Doutor Ricardo Jorge, Porto, Portugal. The original Article has been corrected. [Abstract] The comet assay or single cell gel electrophoresis, is the most common method used to measure strand breaks and a variety of other DNA lesions in human populations. To estimate the risk of overall mortality, mortality by cause, and cancer incidence associated to DNA damage, a cohort of 2,403 healthy individuals (25,978 person-years) screened in 16 laboratories using the comet assay between 1996 and 2016 was followed-up. Kaplan–Meier analysis indicated a worse overall survival in the medium and high tertile of DNA damage (p
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- 2021
13. The hCOMET project: international database comparison of results with the comet assay in human biomonitoring. baseline frequency of DNA damage and effect of main confounders
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Milić, Mirta, Ceppi, Marcello, Bruzzone, Marco, Azqueta, A., Brunborg, Gunnar, Godschalk, Roger W.L., Koppen, Gudrun F., Sardas, Semra, İstinye Üniversitesi, Eczacılık Fakültesi, Eczacılık Meslek Bilimleri Bölümü, Semra Şardaş / 0000-0001-5456-8636, and Sardas, Semra
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Human Biomonitoring ,Pooled Analysis ,Comet Assay ,Biomarkers ,DNA Damage - Abstract
The alkaline comet assay, or single cell gel electrophoresis, is one of the most popular methods for assessing DNA damage in human population. One of the open issues concerning this assay is the identification of those factors that can explain the large inter-individual and inter-laboratory variation. International collaborative initiatives such as the hCOMET project - a COST Action launched in 2016 - represent a valuable tool to meet this challenge. The aims of hCOMET were to establish reference values for the level of DNA damage in humans, to investigate the effect of host factors, lifestyle and exposure to genotoxic agents, and to compare different sources of assay variability. A database of 19,320 subjects was generated, pooling data from 105 studies run by 44 laboratories in 26 countries between 1999 and 2019. A mixed random effect log-linear model, in parallel with a classic meta-analysis, was applied to take into account the extensive heterogeneity of data, due to descriptor, specimen and protocol variability. As a result of this analysis interquartile intervals of DNA strand breaks (which includes alkali-labile sites) were reported for tail intensity, tail length, and tail moment (comet assay descriptors). A small variation by age was reported in some datasets, suggesting higher DNA damage in oldest age-classes, while no effect could be shown for sex or smoking habit, although the lack of data on heavy smokers has still to be considered. Finally, highly significant differences in DNA damage were found for most exposures investigated in specific studies. In conclusion, these data, which confirm that DNA damage measured by the comet assay is an excellent biomarker of exposure in several conditions, may contribute to improving the quality of study design and to the standardization of results of the comet assay in human populations. WOS:000658539600011 34083035 Q1
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- 2021
14. Children's exposure to environmental pollutants and biomarkers of genetic damage
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Neri, Monica, Ugolini, Donatella, Bonassi Stefano, Fucic Aleksandra, Holland, Nina, Knudsen, Lisbeth, Sram, Radim, Ceppi, Marcello, Bocchini Vittorio, and Merlo Domenico Franco
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child wlfare ,environmental pollution ,biological markers ,DNA damage ,review ,meta-analyses ,molecular epidemiology - Abstract
The present review is based on findings from 178 publications retrived through an extensive search of the MedLine/PubMed database for a 25 years time period (1980-2004) and 10 manually identified papers.Among the cytogenetic biomarkers that are frequently used in field studies, chromosome aberrations (CA) and micronuclei (MN) but not sister chromatid exchanges (SCE) were found consistently increased in children exposed to environmental pollutants. Meta-analyses of the studies reporting SCE in cord blood showed similar levels of SCE in exposed and in non-exposed newborns. Exposure to airborne pollutants, soil and drinking water contaminants. mostly increased CA and, to lesser extent, MN levels in children. The effect of exposure to airborne urban pollutants was consistently reported by field studies measuring DNA, albumin and hemoglobin adducts. Prenatal (in utero) and postnatal exposure (environmental tobacco smoke, ETS) to tobacco smoke compounds were associated with increased frequencies of DNA and hematoglobin adducts and CA. The limited number of field studies measuring DNA fragmentation (comet assay) hypoxanthine-guanine phosphoribosyltransferase (HPRT) and the glycophorin A (GPA) mutation frequency in environmentally exposed children precluded a meaningful evaluation of the usefulness of these assay. Meta-analyses performed in children exposed to ETS and in newborns exposed in utero to their mother's smoke showed 1.3 and 7 times higher levels of hemoglobin adducts compared to referent subjects, respectively. These increases are consistent with the epidemiological evidence of higher lung cancer risk reported in adults who had never smoked and were exposed to ETS during childhood and with 7-15 times higher lung cancer risks reported in smokers than in non-smokers. Higher levels of PAH-DNA adducts were found in fetal than in maternal tissue, suggesting a specific susceptibility of the fetus to this class of ubiquitous environmental pollutants. According to these findings, future research and biomonitoring programs on children would greatly benefit from the inclusion of selected biomarkers that could provide biologically based evidence for the identification of intervantion priorities in environmental health.
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- 2005
15. Intra- and inter-laboratory variation in the scoring of micronuclei and nucleoplasmic bridges in binucleated human lymphocytes Results of an international slide-scoring exercise by the HUMN project
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Fenech, Michael, Bonassi, Stefano, Turner, Julie, Ceciliy, Lando, Ceppi, Marcello, Wushou, Peter Chang, Holland, Nina, Kirsch-Volders, Micheline, Zeiger, Errol, Bigatti, Maria Paola, Bolognesi, Claudia, Cai, Jia, DeLuca, Giuseppe, DiGorgio, Marina, Ferguson, Lynette, Fučić, Aleksandra, and Lima, Omar garcia et al.
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micronucleus ,HUMN project ,nucleoplasmic bridges ,scoring ,human lymphocytes ,DNA damage ,variability ,protocol - Abstract
One of the objectives of the HUman MicroNucleus (HUMN) project is to identify the methodological variables that have an importnate impact on micronucleus(MN) or micronucleated (MNed) cell frequencies meausred in human lymphocytes using the cytokinesis-block micronucleus assay. In previous study we had showen that the scoring criteria used were likely to be an important variable. To determinethe extent of residual variation when laboratories scored cells from the same cultures using the same set of standard scoring criteria, an inter-laboratory slide-scoring exercise was performed among 34 laboratories from 21 countries with a total of 51 slides scorers involved. The results of this stdy show that even under these optimised conditions there is a great variation in the MN frequency or MNed cell frequency obtained by individual laboratories and scorers. All laboratories ranked correctly the MNed cell frequency in cells from cultures that were unirradiated, or exposed to 1 or 2 Gy of gamma rays. The study also estimated that the intra-scorer median coefficient of variation for duplicate MNed cell frequency scores is 29% for inexposed cultures and 14 and 11% for cells exposed to 1 and 2 Gy, respectively. These values can be used as a standard for quality or acceptability of data in future studies. Using a Poisson regression model it was estimated that radiation does explained 67% of the varaince, while staining method, cell sample, laboratory and covariance explained 0, 6, 0, 3, 6, 5 and 25, 6% of the variance, respectively, leaving 3, 1% of the variance unexplaned. As part of this exercise, nucleoplasmic bridges were also estimated by the laboratories ; however, inexperience in the use of this biomarker of chromosome rearrangement was reflected in the much greater heterogenity in the data and the unexplained variation estimated by the Poisson model. The results of these indicate clearly that even after standardizing culture and scoring conditions it will be necessary to calibrate scorers and laboratories if MN, MNed and nucleoplasmic bridge frequencies are to be relibly compared among laboratories and among populations.
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- 2003
16. Human Micronucleus Project: International Database comparison for results with the cytokinesis-block micronucleus assay in human lymphocytes: I effect of laboratory protocol,scoring criteria and host factors on the frequency of micronuclei
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Bonassi, Stefano, Fenech, Michael, Lando, Cecilia, Yi-ping, Lin, Ceppi, Marcello, Chang, Wushou Peter, Holland, Nina, Kirsch-Volders, Micheline, Zeiger, Errol, Ban, Sadayuki, Barale, Roberto, Bigatti, Maria Paola, Bolognesi, Claudia, Jia, Cao, Di Gorgio, Marina, Ferguson, Lynnette, Fučić, Aleksandra, Lima, Omar Garcia, Hrelia, Patrizia, Krishnaja Ayyathan, Lee, Tung-Kwang, Migliore, Lucia, Mikhalevich, Ludmila, Mirkova, Ekaterina, Mosesso, Pasquele, Muller, Wolfgang-Ulrich, Odagiri, Youichi, Scarfi, Maria Rosaria, Szabova, Elena, Vorobtsova, Irina, Vral, Anne, and Zijno, Andrea
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cytokinesis-block micronucleus assay ,peripheral blood lymphocytes ,pooled reanalysis ,biomarkers ,DNA damage - Abstract
Micronucleus(MN) expression in peripheral blood lymphocytes is well established as a standard method for monitoring chromosome damage in human populations. The first results of an analysis of pooled data from laboratories using the cytokinesis-block micronucleus(CBMN) assay and participation in the HUMN (Human Micronucleusproject) international collaborative study are presented. The effects of laboratory protocol, scoring criteria, and host factors on baseline micronucleated binucleated cell (MNC) frequency are evaluated, and a reference range of normal values against which future studies may be compared is provided. Primary data from historical records were submitted by 25 laboratories distributed in 16 countries. This resulted ina database of nearly 7000 subjects. Potentially significant differences were present in the methods used by participating laboratories, such as in the type of culture medium, the concentration of cytochalasin B, the percentage of fetal calf serum and in the culture method. Differences in criteria for scoring micronuclei were also evident. The overall median MNC frequency in nonexposed (i.e. normal) subjects was 6,5% and the interquartile range was between 3 and 12%. An increase in MNC frequency with age was evidente in all but two laboratories. The effect of gender, although not so evident in all databases was also present wtih females having a 19% higher level of MNC frequency (95% confidence interval 14-24%).Statistical analysis were performed using random-effects models for correlated data. Our best model, which included exposure to genotoxic factors, host factors, methods and scoring criteria explained 75% of the total variance, with the largest contribution attributed to laboratory methods.
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- 2001
17. Genotoxic effects of occupational exposure to glass fibres - A human biomonitoring study.
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Ceppi, Marcello, Smolkova, Bozena, Staruchova, Marta, Kazimirova, Alena, Barancokova, Magdalena, Volkovova, Katarina, Collins, Andrew, Kocan, Anton, Dzupinkova, Zuzana, Horska, Alexandra, Buocikova, Verona, Tulinska, Jana, Liskova, Aurelia, Mikusova, Miroslava Lehotska, Krivosikova, Zora, Wsolova, Ladislava, Kuba, Daniel, Rundén-Pran, Elise, El Yamani, Naouale, and Longhin, Eleonora Martha
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GLASS fibers , *OCCUPATIONAL exposure , *GENETIC toxicology , *DNA repair , *DNA damage , *POLYCYCLIC aromatic hydrocarbons - Abstract
As part of a large human biomonitoring study, we conducted occupational monitoring in a glass fibre factory in Slovakia. Shopfloor workers (n = 80), with a matched group of administrators in the same factory (n = 36), were monitored for exposure to glass fibres and to polycyclic aromatic hydrocarbons (PAHs). The impact of occupational exposure on chromosomal aberrations, DNA damage and DNA repair, immunomodulatory markers, and the role of nutritional and lifestyle factors, as well as the effect of polymorphisms in metabolic and DNA repair genes on genetic stability, were investigated. The (enzyme-modified) comet assay was employed to measure DNA strand breaks (SBs) and apurinic sites, oxidised and alkylated bases. Antioxidant status was estimated by resistance to H 2 O 2 -induced DNA damage. Base excision repair capacity was measured with an in vitro assay (based on the comet assay). Exposure of workers to fibres was low, but still was associated with higher levels of SBs, and SBs plus oxidised bases, and higher sensitivity to H 2 O 2. Multivariate analysis showed that exposure increased the risk of high levels of SBs by 20%. DNA damage was influenced by antioxidant enzymes catalase and glutathione S-transferase (measured in blood). DNA repair capacity was inversely correlated with DNA damage and positively with antioxidant status. An inverse correlation was found between DNA base oxidation and the percentage of eosinophils (involved in the inflammatory response) in peripheral blood of both exposed and reference groups. Genotypes of XRCC1 variants rs3213245 and rs25487 significantly decreased the risk of high levels of base oxidation, to 0.50 (p = 0.001) and 0.59 (p = 0.001), respectively. Increases in DNA damage owing to glass fibre exposure were significant but modest, and no increases were seen in chromosome aberrations or micronuclei. However, it is of concern that even low levels of exposure to these fibres can cause significant genetic damage. • Exposure of workers to glass fibres was associated with increased levels of DNA damage and higher sensitivity to H 2 O 2. • DNA damage was influenced by catalase activity and glutathione S-transferase levels measured in peripheral blood. • XRCC1 variants rs3213245 and rs25487 were associated with a decrease in the risk of high DNA oxidation damage. • Glass fibre exposure did not affect the levels of chromosome aberrations or micronuclei in exposed workers. [ABSTRACT FROM AUTHOR]
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- 2023
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18. Author Correction: DNA damage in circulating leukocytes measured with the comet assay may predict the risk of death.
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Bonassi, Stefano, Ceppi, Marcello, Møller, Peter, Azqueta, Amaya, Milić, Mirta, Neri, Monica, Brunborg, Gunnar, Godschalk, Roger, Koppen, Gudrun, Langie, Sabine A. S., Teixeira, João Paulo, Bruzzone, Marco, Da Silva, Juliana, Benedetti, Danieli, Cavallo, Delia, Ursini, Cinzia Lucia, Giovannelli, Lisa, Moretti, Silvia, Riso, Patrizia, and Del Bo', Cristian
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DNA damage , *LEUCOCYTES - Published
- 2021
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19. Aberrant Methylation of Hypermethylated-in-Cancer-1 and Exocyclic DNA Adducts in Tobacco Smokers.
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Peluso, Marco E. M., Munnia, Armelle, Bollati, Valentina, Srivatanakul, Petcharin, Jedpiyawongse, Adisorn, Sangrajrang, Suleeporn, Ceppi, Marcello, Giese, Roger W., Boffetta, Paolo, and Baccarelli, Andrea A.
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DNA methylation ,HEALTH of cigarette smokers ,DNA damage ,TOBACCO smoke ,EPIGENETICS ,HUMAN abnormalities ,TUMOR proteins ,CYCLIN-dependent kinase inhibitors - Abstract
Tobacco smoke has been shown to produce both DNA damage and epigenetic alterations. However, the potential role of DNA damage in generating epigenetic changes is largely underinvestigated in human studies. We examined the effects of smoking on the levels of DNA methylation in genes for tumor protein p53, cyclin-dependent kinase inhibitor2A, hypermethylated-in-cancer-1 (HIC1), interleukin-6, Long Interspersed Nuclear Element type1, and Alu retrotransposons in blood of 177 residents in Thailand using bisulfite-PCR andpyrosequencing. Then, we analyzed the relationship of this methylation with the oxidative DNA adduct, M1dG (a malondialdehyde adduct), measured by 32P-postlabeling. Multivariate statistical analyses showed that HIC1 methylation levels were significantly increased in smokers compared with nonsmokers (p ≤ .05). A dose response was observed, with the highest HIC1 methylation levels in smokers of ≥ 10 cigarettes/day relative to nonsmokers and intermediate values in smokers of 1–9 cigarettes/day (p for trend ≤ .001). No additional relationships were observed. We also evaluated correlations between M1dG and the methylation changes at each HIC1 CpG site individually. The levels of this adduct in smokers showed a significant linear correlation with methylation at one of the 3 CpGs evaluated in HIC1: hypermethylation at position 1904864340 was significantly correlated with the adduct M1dG (covariate-adjusted regression coefficient (β) = .224 ± .101 [SE], p ≤ .05). No other correlations were detected. Our study extends prior work by others associating hypermethylation of HIC1 with smoking; shows that a very specific hypermethylation event can arise from smoking; and encourages future studies that explore a possible role for M1dG in connecting smoking to this latter hypermethylation. [ABSTRACT FROM AUTHOR]
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- 2014
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20. DNA methylation differences in exposed workers and nearby residents of the Ma Ta Phut industrial estate, Rayong, Thailand.
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Peluso, Marco, Bollati, Valentina, Munnia, Armelle, Srivatanakul, Petcharin, Jedpiyawongse, Adisorn, Sangrajrang, Suleeporn, Piro, Sara, Ceppi, Marcello, Bertazzi, Pier Alberto, Boffetta, Paolo, and Baccarelli, Andrea A
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DNA methylation ,INDUSTRIALIZATION ,AIR pollution ,BIOMECHANICS ,DNA damage - Abstract
Background Adverse biological effects from airborne pollutants are a primary environmental concern in highly industrialized areas. Recent studies linked air pollution exposures with altered blood Deoxyribo-nucleic acid (DNA) methylation, but effects from industrial sources and underlying biological mechanisms are still largely unexplored.Methods The Ma Ta Phut industrial estate (MIE) in Rayong, Thailand hosts one of the largest steel, oil refinery and petrochemical complexes in south-eastern Asia. We measured a panel of blood DNA methylation markers previously associated with air pollution exposures, including repeated elements [long interspersed nuclear element-1 (LINE-1) and Alu] and genes [p53, hypermethylated-in-cancer-1 (HIC1), p16 and interleukin-6 (IL-6)], in 67 MIE workers, 65 Ma Ta Phut residents and 45 rural controls. To evaluate the role of DNA damage and oxidation, we correlated DNA methylation measures with bulky DNA and 3-(2-deoxy-β-D-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M1dG) adducts.Results In covariate-adjusted models, MIE workers, compared with rural residents, showed lower LINE-1 (74.8% vs 78.0%; P < 0.001), p53 (8.0% vs 15.7%; P < 0.001) and IL-6 methylation (39.2% vs 45.0%; P = 0.027) and higher HIC1 methylation (22.2% vs 15.3%, P < 0.001). For all four markers, Ma Ta Phut residents exhibited methylation levels intermediate between MIE workers and rural controls (LINE-1, 75.7%, P < 0.001; p53, 9.0%, P < 0.001; IL-6, 39.8%, P = 0.041; HIC1, 17.8%, P = 0.05; all P-values vs rural controls). Bulky DNA adducts showed negative correlation with p53 methylation (P = 0.01). M1dG showed negative correlations with LINE-1 (P = 0.003) and IL-6 methylation (P = 0.05).Conclusions Our findings indicate that industrial exposures may induce alterations of DNA methylation patterns detectable in blood leucocyte DNA. Correlation of DNA adducts with DNA hypomethylation suggests potential mediation by DNA damage. [ABSTRACT FROM PUBLISHER]
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- 2012
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21. Breast fine-needle aspiration malondialdehyde deoxyguanosine adduct in breast cancer.
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Peluso, Marco, Munnia, Armelle, Risso, Gabriella G., Catarzi, Sandra, Piro, Sara, Ceppi, Marcello, Giese, Roger W., and Brancato, Beniamino
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BREAST cancer ,NEEDLE biopsy ,MALONDIALDEHYDE ,BIOMARKERS ,OXIDATIVE stress ,MULTIVARIATE analysis ,FREE radicals ,DNA damage - Abstract
This study has analysed the generation of 3-(2-deoxy-ββ-D-erythro-pentafuranosyl)pyrimido[1,2-αα]purin-10(3H)-one deoxyguanosine adduct [M
1 dG], a biomarker of oxidative stress and lipid peroxidation, in breast fine-needle aspirate samples of 22 patients with breast cancer, at different clinical stages, in respect to 13 controls. The multivariate analysis show that M1 dG adduct was higher in cases than in controls (Mean Ratio (MR) == 5.26, 95% CI == 3.16--8.77). Increased M1 dG was observed in women with a tumour grade 3 and a pathological diameter 2 (MR == 7.61, 95% CI == 3.91--14.80 and MR == 5.75, 95% CI == 3.13--10.59, respectively). A trend with increasing tumour grade and pathological diameter was present (MR == 1.98, 95% CI == 1.57--2.50 and MR == 2.44, 95% CI == 1.71--3.48, respectively). Not significant effects of age and smoking habit were found (MR == 1.58, 95% CI == 0.92--2.72 and MR == 1.68, 95% CI 0.88--3.20, respectively). An increment over the background frequency of M1 dG can contribute to breast cancer development. Increasing severity of breast tumour can influence DNA damage level. [ABSTRACT FROM AUTHOR]- Published
- 2011
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22. DNA Damage in Pakistani Agricultural Workers Exposed to Mixture of Pesticides.
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BhaIIi, Javed A., Ali, Tayyaba, Asi, M. R., Khalid, Zafar M., Ceppi, Marcello, and Khan, Qaiser M.
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SPRAYING & dusting in agriculture ,PESTICIDE applicators (Persons) ,OCCUPATIONAL diseases ,APPLICATION of pesticides ,WORKPLACE exposure to hazardous substances ,PHYSIOLOGICAL effects of agricultural chemicals ,OCCUPATIONAL hazards ,DNA damage ,GENETIC toxicology ,DISEASES ,SAFETY ,PREVENTION - Abstract
The article presents a cross-sectional study which determines whether occupational exposure to a complex mixture of pesticides is linked to the significant increase of DNA damage in farmers who are chronically exposed to pesticides in open fields. It utilized leucocytes from agriculture workers who were prone to pesticide exposure during the spraying season of cotton crop. It also gathered serum from the subjects for further analysis. It showed that there was a significant damage among exposed subjects wherein smokers have a higher risk. Furthermore, the chronic exposure to pesticides produced DNA damages among pesticide sprayers and suggested that certain monitoring should be done as preventive measures.
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- 2009
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23. DNA adduct formation among workers in a Thai industrial estate and nearby residents
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Peluso, Marco, Srivatanakul, Petcharin, Munnia, Armelle, Jedpiyawongse, Adisorn, Meunier, Aurelie, Sangrajrang, Suleeporn, Piro, Sara, Ceppi, Marcello, and Boffetta, Paolo
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AIR pollution , *AIR quality , *ATMOSPHERIC deposition , *DNA damage , *INDUSTRIAL districts , *BIOCHEMICAL genetics - Abstract
Abstract: The genotoxic effects of air pollutant exposures have been studied in people living and working in Map Ta Phut, Rayong province, Thailand, a site where is located the Map Ta Phut Industrial Estate (MIE) one of the largest steel, refinery and petrochemical complex in the South–Eastern Asia. This was done by the conduction of a transversal study aimed to compare the prevalence of bulky DNA adducts in groups of subjects experiencing various degree of air pollution. DNA adduct analysis was performed in the leukocytes of 201 volunteers by the 32P-postlabelling assay: 79 were workers in the MIE complex, including 24 refinery workers, 40 steel workers and 15 tinplate workers, 72 were people residing downwind in the MIE area and 50 were residents in a control district of the same Rayong province but without industrial exposures. The groups of workers were analyzed separately to evaluate if DNA adduct formation differs by the type of industry. The levels of bulky DNA adducts were 1.17±0.17 (SE) adducts/108 nucleotides in refinery workers, 1.19±0.19 (SE) in steel workers, 0.87±0.17 (SE) in tinplate workers, 0.85±0.07 (SE) in MIE residents and 0.53±0.05 (SE) in district controls. No effects of smoking habits on DNA adducts was found. The multivariate regression analysis shows that the levels of DNA adducts were significantly increased among the individuals living near the MIE industrial complex in respect to those resident in a control district (p <0.05). In the groups of occupationally exposed workers, the highest levels of DNA adducts were found among the workers experiencing an occupational exposure to polycyclic aromatic hydrocarbons, e.g. the steel factory and refinery workers. When we have evaluated if the levels of DNA adducts of the PAH exposed workers were different from those of the MIE residents, a statistical significantly difference was found (p <0.05). Our present study indicates that people living near point sources of industrial air pollution can experiment an excess of DNA adduct formation. The emissions from the MIE complex are the main source of air pollution in this area and can be the cause of such increment in the levels of DNA damage. [Copyright &y& Elsevier]
- Published
- 2008
- Full Text
- View/download PDF
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