Neutrophils amplify the formation of DNA adducts by benzo[a]pyrene in lung target cells.

Borm, Paul J. A.; Knaapen, Ad M.; Schins, Roel P.F.; Godschalk, Roger; Schooten, Frederik‐Jan van

doi:10.1289/ehp.97105s51089

Cited by 45 publications

(22 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, such inflammatory phenomena can influence DNA adduct levels in lung target cells by increasing the biologically effective dose of PAH [27]. This hypothesis is consistent with a previous case-control study where the levels of DNA adducts in individuals with inflammatory diseases were significantly higher than those of controls [28].…”

Section: Resultssupporting

confidence: 87%

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

View full text Add to dashboard Cite

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.

show abstract

Section: Resultssupporting

confidence: 87%

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

View full text Add to dashboard Cite

show abstract

“…Although not significant, this difference may be biologically plausible. In vitro formation of DNA adducts by benzo[a]pyrene (B[a]P) in lung epithelial cells has been shown to be increased in a dose dependent manner by coincubation with human polymorphonuclear leukocytes (PMN) [8]. Similarly, activated PMNs were found to be involved in both oxygenation and covalent binding of B[a]P 7,8-dihydrodiol to DNA [38].…”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory cells may favour lung cancer progression by generating reactive oxygen and nitrogen species, secretion of growth stimulatory cytokines, chemokines and pro-angiogenic factors [7]. In addition, inflammatory cells may influence the formation of DNA adducts [8].…”

Section: Introductionmentioning

confidence: 99%

Interleukin 1 receptor antagonist gene polymorphism and risk of lung cancer: A possible interaction with polymorphisms in the interleukin 1 beta gene

et al. 2005

View full text Add to dashboard Cite

“…A wide range of inflammatory responses, from acute infiltration of the mucosa with PMNs to a submucosal mixed chronic inflammatory infiltrate are recorded. Inflammatory cells and their reactive oxygen metabolites can cause mutagenic effects in lung parenchyma (71) and sustained chronic oxidative injury may lead to a non-lethal modification of normal cellular growth control mechanisms, a mechanism by which non-genotoxic carcinogens may function (72). Moreover, the cytolethal-proliferative response described for nongenotoxic carcinogens (5) could be relevant to the nasal mucosa in Mexico City residents, since in the exposed adult population the data suggest that nasal cell low viabilities go along with the increased cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Cell proliferation in nasal respiratory epithelium of people exposed to urbanpollution

Calderón‐Garcidueñas¹,

Rodrı́guez-Alcaraz²,

Garcı́a³

et al. 1999

Carcinogenesis

View full text Add to dashboard Cite

The nasal passages are a common portal of entry and are a prime site for toxicant-induced pathology. Sustained increases in regenerative cell proliferation can be a significant driving force in chemical carcinogenesis. The atmosphere in Mexico City contains a complex mixture of air pollutants and its residents are exposed chronically and sequentially to numerous toxicants and potential carcinogens. We were concerned that exposure to Mexico City's atmosphere might induce cytotoxicity and increase nasal respiratory epithelial cell proliferation. Nasal biopsies were obtained for DNA cell cycle analysis from 195 volunteers. The control population consisted of 16 adults and 27 children that were residents in a Caribbean island with low pollution. The exposed Mexico City population consisted of 109 adults and 43 children. Sixty-one of the adult subjects were newly arrived in Mexico City and were followed for 25 days from their arrival. Control children, control adult and exposed Mexico City children all had similar percentages of cells in the replicative DNA synthesis phase (S phase) of the cell cycle (%S). A significant increase in %S in nasal epithelial cells was seen in exposed adult residents in Mexico City biopsied at three different dates compared with control adults. Newly arrived adults exhibited a control level of cell turnover at day 2 after coming to the city. However, at days 7, 14 and 25 they exhibited significant increases in %S. These data demonstrate an increased and sustained nasal cell turnover rate in the adult population observable in as little as 1 week of residence in Mexico City. This increase in cell proliferation is in agreement with other reports of induced pathological changes in the nasal passages of Mexico City dwellers. These observations suggest an increased potential risk factor of developing nasal neoplasms for residents of large cities with heavy pollution.

show abstract

Neutrophils amplify the formation of DNA adducts by benzo[a]pyrene in lung target cells.

Cited by 45 publications

References 20 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

Interleukin 1 receptor antagonist gene polymorphism and risk of lung cancer: A possible interaction with polymorphisms in the interleukin 1 beta gene

Cell proliferation in nasal respiratory epithelium of people exposed to urbanpollution

Contact Info

Product

Resources

About