Elevated urinary 8‐hydroxydeoxyguanosine, a biomarker of oxidative stress, and lack of association with antioxidant vitamins in chronic obstructive pulmonary disease

Igishi, Tadashi; Hitsuda, Yutaka; Kato, Kazuhiro; Sako, Takanori; Burioka, Naoto; Yasuda, Kazuhiko; Sano, Hiroyuki; Shigeoka, Yasushi; Nakanishi, Hirofumi; Shimizu, Eiji

doi:10.1046/j.1440-1843.2003.00490.x

Cited by 43 publications

(31 citation statements)

References 22 publications

(46 reference statements)

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“…The models fitted were similar to equation 1 with 8-OHdG levels as the outcome Y ijk and concurrent 1 & 2-AN or 1-AP levels as a time varying exposure Exp ijk in separate models. Models for 8-OHdG were also adjusted for self-reported doctor diagnoses of chronic respiratory conditions (chronic bronchitis, emphysema), which are thought to be associated with oxidative damage [36]. …”

Section: Methodsmentioning

confidence: 99%

Short-Term Traffic-Related Exposures and Biomarkers of Nitro-PAH Exposure and Oxidative DNA Damage

Neophytou

Hart

Chang

et al. 2014

Toxics

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Exposure to vehicle exhaust has been associated with cardiac and respiratory disease, lung cancer, and greater overall mortality. We investigated whether amino- polycyclic aromatic hydrocarbon (amino-PAH) metabolites of nitro-PAHs could be used as biomarkers of these exposures. Pre- and post-shift urine samples were collected at the beginning and end of a work week from 82 male U.S trucking industry workers. We used repeated-measures analysis to examine associations of total 1- and 2-aminonaphthalene (1 & 2-AN) and 1-aminopyrene (1-AP) urinary concentrations with microenvironment exposures to particulate matter (PM2.5), elemental and organic carbon, and between 1&2-AN and 1-AP with urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG). There was an association between work week mean PM2.5 levels and post-shift 1 & 2-AN, [141.8 pg/ml increase (95% CI:53.3, 230.2) for each IQR increase (5.54 µg/m3) in PM2.5,] but no associations with other exposure measures. There was a statistically significant increase in 8-OHdG concentrations with 1 & 2-AN (2.38 µg/mg creatinine (95%CI: 0.19, 4.58) per 242.85 pg/mg creatinine increase in 1 & 2-AN), and suggestive associations with all other exposure measures. Our findings suggest associations between urinary amino-PAHs with vehicle exhaust related PM2.5 as well as with a biomarker of oxidative DNA damage.

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Section: Methodsmentioning

confidence: 99%

Short-Term Traffic-Related Exposures and Biomarkers of Nitro-PAH Exposure and Oxidative DNA Damage

Neophytou

Hart

Chang

et al. 2014

Toxics

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“…Several studies have identified markers of free radical damage are present in patients with COPD. Increased levels of urinary 8-OH-dG have been detected in the urine of COPD patients [18] and elevated levels of 3-nitrotyrosine [19] and lung lipid peroxidation products [20] are detected in the airway cells and epithelium of COPD patients. All of these oxidative markers had an inverse correlation with lung function suggesting that they could be key mediators of the physiologic deterioration that is noted in patients with this disease.…”

Section: Evidence For Oxidative Damage In Copd and Asthmamentioning

confidence: 99%

The effect of cigarette smoke–derived oxidants on the inflammatory response of the lung

Foronjy

DʼArmiento

2006

Clinical and Applied Immunology Reviews

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The inhalation of cigarette smoke triggers a marked cellular influx in the lung and this inflammation is believed to play a central role in the development of smoke-related lung diseases such as asthma and COPD. Studies demonstrate that smoke-derived oxidants are a major factor in this inflammatory reaction to cigarette smoke. These oxidants can overwhelm the lung's antioxidant defenses and they can up regulate inflammation by a number of mechanisms. Free radicals directly stimulate the production of chemotactic compounds such as 8-isoprostane. In addition, smoke-derived oxidants can activate several intracellular signaling cascades including NF-κB, MAPK and AP-1. This transcriptional activation induces the expression of cytokines and intracellular adhesion molecules that facilitates the trafficking of neutrophils, macrophages and lymphocytes into the lung. Moreover, oxidants can promote chromatin remodeling that facilitates the expression of proinflammatory genes by stimulating the acetylation of histone residues in the nucleosome. This leads to conformational changes that enhance expression by rendering the gene more accessible to binding to transcriptional factors. Thus, the oxidant-antioxidant imbalance generated by cigarette smoke can promote inflammation which is critical to the functional decline that occurs in both asthma and COPD patients. Future research is needed to better define the effects of smoke-derived oxidants on lung inflammation and to determine the most efficacious strategies for generating significant antioxidant protection in the lung.

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“…other study reported that urinary desmosine, a marker of mature elastin degradation, was found to be increased in smokers with rapid decline in lung function [99][100] and furthermore elevated in acute COPD exacerbation [106]. In addition, urinary desmosine excretion appeared significantly elevated in patients with COPD compared to controls, and particularly in patients with moderate to severe emphysema measured by high resolution computed tomography [102].…”

Section: Serum C-reactive Protein (Crp)mentioning

confidence: 90%

Biomarkers in COPD

Tzortzaki¹,

Lambiri²,

Vlachaki³

et al. 2007

CMC

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Chronic Obstructive Pulmonary Disease is characterized by an abnormal inflammatory response of the lungs to noxious particles and gases, caused primarily by cigarette smoking. Although COPD affects the lung, it also produces significant systemic consequences. Inflammation, proteases-antiproteases imbalance, oxidative stress, tissue damage and tissue repair, apoptosis and several genes seem to be involved in the pathogenesis of the disease. The cellular and molecular events underlying COPD pathogenesis are driven by multifunctional molecules including enzymes, cytokines, chemokines, growth factors, lipid mediators and their respective receptors. A large number of biomarkers evaluated in COPD, showed a high degree of redundancy. Nevertheless, current understanding of the pathobiology of COPD suggests a number of biomarkers as potential candidates. The development of relevant markers of lung damage, pulmonary inflammation, and systemic disease will be essential to our further understanding of the natural history of COPD and the discovery of new, effective treatments for its progression. This review summarizes recent findings, on potential pulmonary biomarkers in the induced sputum, the exhaled air condensate, the peripheral blood, the urine, the bronchoalveolar lavage fluid, and in selective cases, in bronchial biopsies.

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Elevated urinary 8‐hydroxydeoxyguanosine, a biomarker of oxidative stress, and lack of association with antioxidant vitamins in chronic obstructive pulmonary disease

Cited by 43 publications

References 22 publications

Short-Term Traffic-Related Exposures and Biomarkers of Nitro-PAH Exposure and Oxidative DNA Damage

Short-Term Traffic-Related Exposures and Biomarkers of Nitro-PAH Exposure and Oxidative DNA Damage

The effect of cigarette smoke–derived oxidants on the inflammatory response of the lung

Biomarkers in COPD

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