ROS in the local and systemic pathogenesis of COPD

Langen, Ramon; Korn, S; Wouters, Emiel F.M.

doi:10.1016/s0891-5849(03)00316-2

Cited by 129 publications

(92 citation statements)

References 104 publications

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“…8-Iso-PGF 2a of healthy subjects range from 0.27 to 3.5 pg/mg creatinine (determined with EIA) (Engler et al, 2004). These values are usually increased in COPD patients (Praticò et al, 1998) since reactive oxygen species (ROS) are involved in the evolution and pathophysiology of this disease (Langen et al, 2003). Data regarding the effect of polyphenol antioxidants on isoprostane concentration are apparently contradictory in the literature.…”

Section: Discussionmentioning

confidence: 99%

“…Cigarette smoke provides a huge concentration of reactive oxygen species (ROS) that critically contribute to provoke systemic oxidative stress (Rahman et al, 1996). Several studies support the role of ROS in the evolution and pathophysiology of obstructive airway diseases including COPD (Macnee, 2000;Langen et al, 2003;Molfino, 2004). As oxidative stress is increased in patients with COPD (Praticò et al, 1998), antioxidants could be of use in its treatment.…”

Section: Introductionmentioning

confidence: 99%

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Pomegranate juice supplementation in chronic obstructive pulmonary disease: a 5-week randomized, double-blind, placebo-controlled trial

et al. 2005

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Objective: The aim of the present study is to investigate the effect of antioxidant polyphenol-rich pomegranate juice (PJ) supplementation for 5 weeks on patients with stable chronic obstructive pulmonary disease (COPD), since the oxidative stress plays a major role in the evolution and pathophysiology of COPD. Design: A randomized, double-blind, placebo-controlled trial was conducted. Subjects: A total of 30 patients with stable COPD were randomly distributed in two groups (15 patients each). Interventions: Both groups consumed either 400 ml PJ daily or matched placebo (synthetic orange-flavoured drink) for 5 weeks. Trolox Equivalent Antioxidant Capacity (TEAC) of PJ, blood parameters (14 haematological and 18 serobiochemical), respiratory function variables, bioavailability of PJ polyphenols (plasma and urine) and urinary isoprostane (8-iso-PGF 2a ) were evaluated. Results: The daily dose of PJ (containing 2.66 g polyphenols) provided 4 mmol/l TEAC. None of the polyphenols present in PJ were detected in plasma or in urine of volunteers. The most abundant PJ polyphenols, ellagitannins, were metabolized by the colonic microflora of COPD patients to yield two major metabolites in both plasma and urine (dibenzopyranone derivatives) with no TEAC. No differences were found (P40.05) between PJ and placebo groups for any of the parameters evaluated (serobiochemical and haematological), urinary 8-iso-PGF 2a , respiratory function variables and clinical symptoms of COPD patients. Conclusions: Our results suggest that PJ supplementation adds no benefit to the current standard therapy in patients with stable COPD. The high TEAC of PJ cannot be extrapolated in vivo probably due to the metabolism of its polyphenols by the colonic microflora. The understanding of the different bioavailability of dietary polyphenols is critical before claiming any antioxidantrelated health benefit. Sponsorship: 'Fundació n Séneca' (Murcia, Spain), Project PB/18/FS/02 and Spanish CICYT, Project AGL2003-02195.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pomegranate juice supplementation in chronic obstructive pulmonary disease: a 5-week randomized, double-blind, placebo-controlled trial

et al. 2005

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“…This can lead to airway obstruction and chronic obstructive pulmonary disease (COPD). 2 The oxidative stress hypothesis may explain why smokers have a higher risk of COPD; they are exposed to cigarette smoke, which contains high concentrations of oxidants such as reactive oxygen species (ROS). 2 3 However, smoking usually results in COPD in only 15-20% of smokers, 4 suggesting a genetic susceptibility to lung function decline and to the development of COPD in smokers.…”

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confidence: 99%

Association of lung function decline with the heme oxygenase-1 gene promoter microsatellite polymorphism in a general population sample. Results from the European Community Respiratory Health Survey (ECRHS), France

Guénégou¹,

Leynaert²,

Bénessiano³

et al. 2006

Journal of Medical Genetics

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Inducible heme oxygenase (HO-1) acts against oxidants that are thought to play a major role in the pathogenesis of chronic obstructive pulmonary disease (COPD), characterised by impaired lung function. A (GT) n repeat polymorphism in the HO-1 gene promoter can modulate the gene transcription in response to oxidative stress. We hypothesised that this polymorphism could be associated with the level of lung function and decline in subjects exposed to oxidative agression (smokers). We genotyped 749 French subjects (20-44 years, 50% men, 40% never smokers) examined in both 1992 and 2000 as part of the ECRHS. Lung function was assessed by forced expiratory volume in 1 second (FEV 1 ) and FEV 1 /forced ventilatory capacity (FVC) ratio. We compared long (L) allele carriers ((GT) n >33 repeats for one or two alleles) to non-carriers. Cross sectionally, in 2000, L allele carriers showed lower FEV 1 / FVC than non-carriers. During the 8 year period, the mean annual FEV 1 and FEV 1 /FVC declines were 230.9 (31.1) ml/ year and 21.8 (6.1) U/year, respectively. FEV 1 /FVC decline was steeper in L allele carriers than in non-carriers (22.6 (5.5) v 21.5 (6.4), p = 0.07). There was a strong interaction between the L allele and smoking. In 2000, the L allele was associated with lower FEV 1 and FEV 1 /FVC in heavy smokers (>20 cigarettes/day) only (p for interaction = 0.07 and 0.002 respectively). Baseline heavy smokers carrying the L allele showed the steepest FEV 1 decline (262.0 (29.5 ml/year) and the steepest FEV 1 /FVC decline (28.8 (5.4 U/year) (p for interaction = 0.009 and 0.0006).These results suggest that a long (L) HO-1 gene promoter in heavy smokers is associated with susceptibility to develop airway obstruction.

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“…The pathogenesis of COPD has been strongly associated with reactive oxygen species [1-4], although it is not known how oxidative/nitrosative stress predicts the disease progression. Several oxidant markers and ''footprints'' of oxidative/nitrosative damage have been detected in COPD lung tissue, sputum, exhaled air and exhaled breath condensate [3][4][5][6], but it has not been unequivocally resolved whether these biomarkers can be used in the early assessment of cigarette-smoke-related lung diseases, their progression or whether they relate to smoking alone.8-Epi-prostaglandinF 2a (8-isoprostane) has been suggested to be the most reliable approach to monitor oxidative stress in vivo [7,8]. Isoprostanes are formed by free-radical-catalysed lipid peroxidation of arachidonic acid and cell membrane phospholipids.…”

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confidence: 99%

8-Isoprostane as a marker of oxidative stress in nonsymptomatic cigarette smokers and COPD

Kinnula¹,

Ilumets²,

Myllärniemi³

et al. 2006

Eur Respir J

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8-Isoprostane is a potential in vivo marker for oxidant burden, but its usefulness in induced sputum of smokers and chronic obstructive pulmonary disease (COPD) has not been investigated.The current study investigated 58 subjects comprising 11 never-smokers, 11 ex-smokers, 13 healthy current smokers and 23 COPD with stage 0-III disease (according to the Global Initiative for Chronic Obstructive Lung Disease criteria). 8-Isoprostane was determined from induced sputum by enzyme immunoassay.Sputum 8-isoprostane levels were similar in the never-smokers and ex-smokers, but were elevated in the healthy smokers compared with nonsmokers, and in those with stage I-III COPD. Sputum 8-isoprostane levels could not differentiate nonsymptomatic smokers from those with Stage 0 COPD. There was a correlation between sputum 8-isoprostane level and lung function parameters (forced expiratory volume in one second/forced vital capacity and sputum neutrophils.In conclusion, sputum 8-isoprostane levels correlate with the severity of chronic obstructive pulmonary disease. However, they do not appear to differentiate healthy smokers from those who are at risk of developing chronic obstructive pulmonary disease (Global Initiative for Chronic Obstructive Lung Disease stage 0). KEYWORDS: Chronic obstructive pulmonary disease, cigarette smoking, oxidant, sputum C hronic obstructive pulmonary disease (COPD) is generally diagnosed when lung function parameters have become significantly reduced and a major part of the lung has been damaged. The pathogenesis of COPD has been strongly associated with reactive oxygen species [1-4], although it is not known how oxidative/nitrosative stress predicts the disease progression. Several oxidant markers and ''footprints'' of oxidative/nitrosative damage have been detected in COPD lung tissue, sputum, exhaled air and exhaled breath condensate [3][4][5][6], but it has not been unequivocally resolved whether these biomarkers can be used in the early assessment of cigarette-smoke-related lung diseases, their progression or whether they relate to smoking alone.8-Epi-prostaglandinF 2a (8-isoprostane) has been suggested to be the most reliable approach to monitor oxidative stress in vivo [7,8]. Isoprostanes are formed by free-radical-catalysed lipid peroxidation of arachidonic acid and cell membrane phospholipids. Isoprostanes can also be released into the circulation, secretions and urine where levels have been found to be stable and reproducible in many experimental approaches [8,9]. Isoprostanes also have potent biological actions and therefore they may significantly contribute to the progression of oxidant-mediated lung diseases, such as COPD.Several studies have shown elevated 8-isoprostane in the exhaled breath condensate of COPD patients [10][11][12][13]. There are, however, a number of uncertainties with respect to the usefulness and standardisation of exhaled breath condensate [14][15][16][17]. One recent study also failed to detect 8-isoprostane in exhaled breath condensate in the majority o...

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ROS in the local and systemic pathogenesis of COPD

Cited by 129 publications

References 104 publications

Pomegranate juice supplementation in chronic obstructive pulmonary disease: a 5-week randomized, double-blind, placebo-controlled trial

Pomegranate juice supplementation in chronic obstructive pulmonary disease: a 5-week randomized, double-blind, placebo-controlled trial

Association of lung function decline with the heme oxygenase-1 gene promoter microsatellite polymorphism in a general population sample. Results from the European Community Respiratory Health Survey (ECRHS), France

8-Isoprostane as a marker of oxidative stress in nonsymptomatic cigarette smokers and COPD

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