Comparison between smoking-related DNA adduct analysis in induced sputum and peripheral blood lymphocytes

Nia, Ahmad Besarati; Maas, L.M.; Brouwer, E.M.; Kleinjans, Jos; Schooten, Frederik J. van

doi:10.1093/carcin/21.7.1335

Cited by 29 publications

(8 citation statements)

References 28 publications

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“…Our aim was to evaluate whether the levels of DNA adducts were associated with benign or malignant lung chronic diseases. The question of the utility of PBLs as a valid surrogate for a specific organ like lung, representing the events occurring in the target tissue, is still open [19]. Nevertheless, some studies have indicated that the use of PBLs such as a biological marker, may help in the identification of subjects at elevated risk [6–8].…”

Section: Resultsmentioning

confidence: 99%

Smoking, DNA Adducts and Number of Risk DNA Repair Alleles in Lung Cancer Cases, in Subjects with Benign Lung Diseases and in Controls

Peluso

Munnia

Piro

et al. 2010

Journal of Nucleic Acids

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Smoke constituents can induce DNA adducts that cause mutations and lead to lung cancer. We have analyzed DNA adducts and polymorphisms in two DNA repair genes, for example, XRCC1 Arg194Trp and Arg399Gln genes and XRCC3 Thr241Met gene, in 34 lung cancer cases in respect to 30 subjects with benign lung cancer disease and 40 healthy controls. When the study population was categorized in base to the number of risk alleles, adducts were significantly increased in individuals bearing 3-4 risk alleles (OR = 4.1 95% C.I. 1.28–13.09, P = .009). A significant association with smoking was noticed in smokers for more than 40 years carrying 3-4 risk alleles (OR = 36.38, 95% C.I. 1.17–1132.84, P = .040). A not statistically significant increment of lung cancer risk was observed in the same group (OR = 4.54, 95% C.I. 0.33–62.93, P = .259). Our results suggest that the analysis of the number of risk alleles predicts the interindividual variation in DNA adducts of smokers and lung cancer cases.

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Section: Resultsmentioning

confidence: 99%

Smoking, DNA Adducts and Number of Risk DNA Repair Alleles in Lung Cancer Cases, in Subjects with Benign Lung Diseases and in Controls

Peluso

Munnia

Piro

et al. 2010

Journal of Nucleic Acids

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“…Several studies have attempted to assess the effect of smoking on PAH‐DNA adduct formation in total peripheral white blood cells, but the results have been inconsistent between studies. A few studies have shown an association between PAH‐DNA adduct levels and smoking 37, 38, 39, 40. Mooney et al 41.…”

Section: Discussionmentioning

confidence: 99%

DNA bulky adducts in a Mediterranean population correlate with environmental ozone concentration, an indicator of photochemical smog

Palli

Saieva

Grechi

et al. 2003

Intl Journal of Cancer

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1 Ozone (O 3 ), the major oxidant component in photochemical smog, mostly derives from photolysis of nitrogen dioxide. O 3 may have biologic effects directly and/or via free radicals reacting with other primary pollutants and has been reported to influence daily mortality and to increase lung cancer risk. Although DNA damage may be caused by ozone itself, only other photochemical reaction products (as oxidised polycyclic aromatic hydrocarbons) may form bulky DNA adducts, a reliable biomarker of genotoxic damage and cancer risk, showing a seasonal trend. In a large series consisting of 320 residents in the metropolitan area of Florence, Italy, enrolled in a prospective study for the period 1993-1998 (206 randomly sampled volunteers, 114 traffic-exposed workers), we investigated the correlation between individual levels of DNA bulky adducts and a cumulative O 3 exposure score. The average O 3 concentrations were calculated for different time windows (0 -5 to 0 -90 days) prior to blood drawing for each participant, based on daily measurements provided by the local monitoring system. Significant correlations between DNA adduct levels and O3 cumulative exposure scores in the last 2-8 weeks before enrollment emerged in never smokers. Correlations were highest in the subgroup of never smokers residing in the urban area and not occupationally exposed to vehicle traffic pollution, with peak values for average concentrations 4 -6 weeks before enrollment (r ‫؍‬ 0.34). Our current findings indicate that DNA adduct formation may be modulated by individual characteristics and by the cumulative exposure to environmental levels of ozone in the last 4 -6 weeks, possibly through ozone-associated reactive pollutants.

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“…Adducts are identified either as spots on thin layer chromatography plates observed by autoradiographic detection or as peaks using high-performance liquid chromatography (HPLC) separation with radioactive detection. This method has been successfully employed to screen for DNA adducts in a variety of human tissues and white blood cells [ 18 , 19 , 20 , 21 , 22 , 23 ], in exfoliated epithelial cells in urine of smokers [ 24 ], in breast milk of lactating mothers [ 25 ], and the sputum of lung cancer patients [ 26 , 27 ]. These studies have revealed that human DNA is modified by many different electrophiles, including those formed endogenously as well as by both environmental and dietary genotoxicants.…”

Section: Conventional Approach For Dna Adduct Screening: mentioning

confidence: 99%

The Future of DNA Adductomic Analysis

Villalta

Balbo

2017

IJMS

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Covalent modification of DNA, resulting in the formation of DNA adducts, plays a central role in chemical carcinogenesis. Investigating these modifications is of fundamental importance in assessing the mutagenicity potential of specific exposures and understanding their mechanisms of action. Methods for assessing the covalent modification of DNA, which is one of the initiating steps for mutagenesis, include immunohistochemistry, 32P-postlabeling, and mass spectrometry-based techniques. However, a tool to comprehensively characterize the covalent modification of DNA, screening for all DNA adducts and gaining information on their chemical structures, was lacking until the recent development of “DNA adductomics”. Advances in the field of mass spectrometry have allowed for the development of this methodology. In this perspective, we discuss the current state of the field, highlight the latest developments, and consider the path forward for DNA adductomics to become a standard method to investigate covalent modification of DNA. We specifically advocate for the need to take full advantage of this new era of mass spectrometry to acquire the highest quality and most reliable data possible, as we believe this is the only way for DNA adductomics to gain its place next to the other “-omics” methodologies as a powerful bioanalytical tool.

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Comparison between smoking-related DNA adduct analysis in induced sputum and peripheral blood lymphocytes

Cited by 29 publications

References 28 publications

Smoking, DNA Adducts and Number of Risk DNA Repair Alleles in Lung Cancer Cases, in Subjects with Benign Lung Diseases and in Controls

Smoking, DNA Adducts and Number of Risk DNA Repair Alleles in Lung Cancer Cases, in Subjects with Benign Lung Diseases and in Controls

DNA bulky adducts in a Mediterranean population correlate with environmental ozone concentration, an indicator of photochemical smog

The Future of DNA Adductomic Analysis

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