Imbalance between levels of nitrogen oxides and peroxynitrite inhibitory activity in chronic obstructive pulmonary disease

Kanazawa, Hiroshi; Shiraishi, Satoshi; Hirata, Kazuto; Yoshikawa, Junichi

doi:10.1136/thorax.58.2.106

Cited by 43 publications

(35 citation statements)

References 23 publications

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“…The reason why exhaled NO may be elevated in COPD as much as in asthma may be because exhaled NO levels are depressed by cigarette smoking and oxidative stress, since NO combines avidly with superoxide anions to form peroxynitrite. This is supported by the fact that nitrate concentrations, formed by metabolism of peroxynitrite, are increased in breath condensate and sputum of cigarette smokers and patients with COPD (Corradi et al, 2001;Kanazawa et al, 2003c). Generation of superoxide anions from neutrophils also decreases the amount of NO formed by an epithelial cell line in vitro, as NO is consumed to form peroxynitrite .…”

Section: Nitric Oxidementioning

confidence: 91%

“…Generation of superoxide anions from neutrophils also decreases the amount of NO formed by an epithelial cell line in vitro, as NO is consumed to form peroxynitrite . There is also a reduction in the undefined "peroxynitrite inhibitory activity" in sputum of COPD patients (Kanazawa et al, 2003c). Peroxynitrite reacts with tyrosine residues in certain proteins to form 3-nitrotyrosine, which may be detected immunologically.…”

Section: Nitric Oxidementioning

confidence: 99%

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Mediators of Chronic Obstructive Pulmonary Disease

2004

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Section: Nitric Oxidementioning

confidence: 91%

Section: Nitric Oxidementioning

confidence: 99%

Mediators of Chronic Obstructive Pulmonary Disease

2004

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“…A recent study by KANAZAWA et al [40] has shown that increased levels of NO and reduced peroxynitrite inhibitory activity were present in induced sputum from patients with COPD. The increased level of RNS was inhibited following steroid therapy in patients with COPD, and the reduction in nitrotyrosine and iNOS immunoreactivity in sputum cells was correlated with the improvement in FEV1 and airway responsiveness to histamine [41].…”

Section: Oxidative Stress In Bloodmentioning

confidence: 99%

Oxidative stress and redox regulation of lung inflammation in COPD

Rahman

Adcock²

2006

Eur Respir J

783

599

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Reactive oxygen species, either directly or via the formation of lipid peroxidation products, may play a role in enhancing inflammation through the activation of stress kinases (cJun activated kinase, extracellular signal-regulated kinase, p38) and redox-sensitive transcription factors, such as nuclear factor (NF)-kB and activator protein-1. This results in increased expression of a battery of distinct pro-inflammatory mediators. Oxidative stress activates NF-kBmediated transcription of pro-inflammatory mediators either through activation of its activating inhibitor of kB-a kinase or the enhanced recruitment and activation of transcriptional coactivators. Enhanced NF-kB-co-activator complex formation results in targeted increases in histone modifications, such as acetylation leading to inflammatory gene expression.Emerging evidence suggests the glutathione redox couple may entail dynamic regulation of protein function by reversible disulphide bond formation on kinases, phosphatases and transcription factors. Oxidative stress also inhibits histone deacetylase activity and in doing so further enhances inflammatory gene expression and may attenuate glucocorticoid sensitivity.The antioxidant/anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn, erdosteine), dietary polyphenols (curcumin-diferuloylmethane, cathechins/ quercetin and reserveratol), specific spin traps, such as a-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (extracellular superoxide dismutase (SOD) mimetic, SOD mimetic M40419 and SOD, and catalase manganic salen compound, eukarion-8), porphyrins (AEOL 10150 and AEOL 10113) and theophylline have all been shown to play a role in either controlling NF-kB activation or affecting histone modifications with subsequent effects on inflammatory gene expression in lung epithelial cells.Thus, oxidative stress regulates both key signal transduction pathways and histone modifications involved in lung inflammation. Various approaches to enhance lung antioxidant capacity and clinical trials of antioxidant compounds in chronic obstructive pulmonary disease are also discussed.

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“…Nitroxidative stress is indeed increased in COPD, and inhibition of inducible nitric oxide synthase protects mice from smoke-induced emphysema and pulmonary hypertension [87][88][89][90]. When folic acid is administered in supraphysiologic doses, high intracellular concentrations of tetrahydrofolates accumulate in most cells, and can exert potent oxidant scavenging effects most notably, scavenging of peroxynitrite -derived radicals [91,92].…”

Section: Adjuvant Strategies Targeting Nrf2mentioning

confidence: 99%

DHA May Have a Profoundly Protective Impact on the Lungs of Smokers

Mf¹

2016

J Nutr Food Sci

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Evidence has accumulated over the last twenty years that smokers who frequently ingest fish are at lower risk for both chronic obstructive pulmonary disease (COPD) and lung cancer. Plasma phospholipid levels of DHA, but not EPA, have been reported to correlate inversely with risk for COPD in smokers, suggesting that DHA may be primarily responsible for the apparent protection afforded to lungs of smokers by fish consumption. Meanwhile, evidence is emerging that certain metabolites of DHA -including 4 -hydroxy hexenal (4-HHE), 17 -oxo -DHA, and resolvin D1 -can activate Nrf2 -mediated transcription of heme oxygenase -1 and other antioxidant / cytoprotective enzymes. Since the oxidant stress imposed by cigarette smoke exposure could be expected to promote peroxidation of membrane DHA and hence boost production of 4 -HHE, DHA in lung membranes may in effect up-regulate the protective feedback mechanism whereby oxidative stress provokes Nrf2 -mediated induction of cytoprotective enzymes. DHA can also give rise to the autacoid resolvin D1, which, via activation of a receptor, suppresses NFkappaB activation and the consequent production of pro-inflammatory cytokines. Resolvin D1 can also inhibit macrophage NADPH oxidase and promote an anti-inflammatory M2 phenotype in lung macrophages. Not surprisingly, inhalation of resolvin D1 has a marked anti-inflammatory impact on the lungs of mice exposed to tobacco smoke. These considerations help to rationalize the epidemiology linking fish consumption to lung health, and suggest that smokers who can't or won't quit their habit would be well advised to consume fish or DHA supplements regularly. Higher intakes of fruits and vegetables -likely in part because many of these contain Nrf2 -activating phytochemicals -likewise are associated with lower risk for COPD, and can be recommended for smokers.Keywords: COPD; Lung cancer; Fish; Docosahexaenoic acid (DHA); 4 -hydroxy hexenal; Nrf2; Resolvin D1 Fish Consumption May Protect Smokers from COPDLimited but nonetheless compelling epidemiology has linked heavy dietary consumption of fresh fish to marked decreases in risk for lung cancer and chronic obstructive pulmonary disease (COPD) among smokers. The first key evidence in this regard emerged in 1994. Shahar et al.[1] studied subjects enrolled in the prospective Atherosclerosis Risk in Communities (ARIC) study, who had received a dietary assessment and a physical exam including lung spirometry, and had been questioned regarding lung symptoms [1]. COPD was defined by three separate criteria: self -reported symptoms of chronic bronchitis, physician diagnosis of emphysema, and via spirometry (FEV1 < 65% of predicted value). When risk for COPD was compared between the first and fourth quartiles of estimated daily intake of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA), relative risk for COPD in the fourth quartile (mean omega-3 intake 480 mg) after appropriate multivariate adjustments was found to be 0.66 (95% CI 0.52 -0.85), 0.31 (CI 0.18 -0.52), and 0.50 (CI 0.32...

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Imbalance between levels of nitrogen oxides and peroxynitrite inhibitory activity in chronic obstructive pulmonary disease

Cited by 43 publications

References 23 publications

Mediators of Chronic Obstructive Pulmonary Disease

Mediators of Chronic Obstructive Pulmonary Disease

Oxidative stress and redox regulation of lung inflammation in COPD

DHA May Have a Profoundly Protective Impact on the Lungs of Smokers

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