Oxidative Stress and Lung Function

Muti, Paola; Freudenheim, Jo L.; Armstrong, Donald; Browne, Richard W.; Klocke, Robert A.; Trevisan, Maurizio

doi:10.1093/oxfordjournals.aje.a009220

Cited by 108 publications

(84 citation statements)

References 55 publications

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“…In this sample of patients with chronic airflow limitation and in our previous study of healthy individuals, we found a statistically significant inverse association of glutathione and FEV 1 (Schünemann et al, 1997). We speculate that an inverse selection is meaningful, as the body attempts to compensate for lower levels of glutathione in tissues during more severe disease.…”

Section: Discussionsupporting

confidence: 60%

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Antioxidants, oxidative stress, and pulmonary function in individuals diagnosed with asthma or COPD

et al. 2006

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Objective: The objective of this study was to investigate the association between antioxidant nutrients and markers of oxidative stress with pulmonary function in persons with chronic airflow limitation. Design: Cross-sectional study exploring the association of antioxidant nutrients and markers of oxidative stress with forced expiratory volume in the first second (FEV 1 %) and forced vital capacity (FVC%). Setting/Subjects: The study data included 218 persons with chronic airflow limitation recruited randomly from the general population of Erie and Niagara counties, New York State, USA. Results: After adjustment for covariates, multiple linear regression analysis showed that serum b-cryptoxanthin, lutein/ zeaxanthin, and retinol, and dietary b-carotene, b-cryptoxanthin, lutein/zeaxanthin, vitamin C, and lycopene were positively associated with FEV 1 % (Po0.05, all associations). Serum vitamins b-cryptoxanthin, lutein/zeaxanthin, and lycopene, and dietary b-cryptoxanthin, b-carotene, vitamin C, and lutein/zeaxanthin were positively associated with FVC% (Po0.05, all associations). Erythrocytic glutathione was negatively associated with FEV 1 %, while plasma thiobarbituric acid-reactive substances (TBARS) were negatively associated with FVC% (Po0.05). Conclusion: These results support the hypothesis that an imbalance in antioxidant/oxidant status is associated with chronic airflow limitation, and that dietary habits and/or oxidative stress play contributing roles.

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Section: Discussionsupporting

confidence: 60%

“…We found a negative association of FEV 1 % and TBARS, a marker for lipid peroxidation (Schünemann et al, 1997). In the current analysis, we found a negative association of TBARS with FVC, but not with FEV 1 .…”

Section: Discussioncontrasting

confidence: 53%

Antioxidants, oxidative stress, and pulmonary function in individuals diagnosed with asthma or COPD

et al. 2006

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“…Increasing age is highly associated with increased oxidative stress (Romano et al 2010;Schunemann et al 1997). Therefore, we anticipated that the aged lung would represent a relatively oxidized environment.…”

Section: Alf In Old Age Contains Increased Myeloperoxidase and Oxidizmentioning

confidence: 99%

“…Therefore, slow ALF turnover plus the presence of inflammatory lung and parenchymal cells can drive baseline low-grade chronic inflammation in the lung during aging (Reynolds 1987). These events result in changes in alveolar surfactant and complement production and activity, the former as a result of a change in the local oxidation state (Schunemann et al 1997). Moreover, alterations in surfactant lipid composition are predicted to negatively affect SP-A and SP-D function (Veldhuizen et al 1998), and the latter proteins can be oxidized themselves (Umstead et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Molecular composition of the alveolar lining fluid in the aging lung

Moliva

Rajaram

Sidiki

et al. 2014

AGE

103

121

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As we age, there is an increased risk for the development of pulmonary diseases, including infections, but few studies have considered changes in lung surfactant and components of the innate immune system as contributing factors to the increased susceptibility of the elderly to succumb to infections. We and others have demonstrated that human alveolar lining fluid (ALF) components, such as surfactant protein (SP)-A, SP-D, complement protein C3, and alveolar hydrolases, play a significant innate immune role in controlling microbial infections. However, there is a lack of information regarding the effect of increasing age on the level and function of ALF components in the lung. Here we addressed this gap in knowledge by determining the levels of ALF components in the aging lung that are important in controlling infection. Our findings demonstrate that pro-inflammatory cytokines, surfactant proteins and lipids, and complement components are significantly altered in the aged lung in both mice and humans. Further, we show that the aging lung is a relatively oxidized environment. Our study provides new information on how the pulmonary environment in old age can potentially modify mucosal immune responses, thereby impacting pulmonary infections and other pulmonary diseases in the elderly population.

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“…Schunemann et al (1997) were the first to report an inverse correlation between plasma lipid peroxidation products and lung functions. However, the studies on the relationships between oxidant/antioxidant imbalance and pulmonary functions did not yield consistent results.…”

Section: Relationships Between Oxidative Stress and Pulmonary Functionsmentioning

confidence: 99%

The role of oxidative stress in lung injury induced by cigarette smoke

Kluchová

Tkáčová

2006

Biologia

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Oxidative stress is a damaging process resulting from an imbalance between excessive generation of oxidant compounds and insufficient antioxidant defence mechanisms. Oxidative stress plays a crucial role in the initiation and progression of cigarette smoke-induced lung injury, deterioration in lung functions, and development of chronic obstructive pulmonary disease (COPD). In smokers and in patients with COPD, the increased oxidant burden derives from cigarette smoke per se, and from activated inflammatory cells releasing enhanced amounts of reactive oxygen and nitrogen species (ROS, RNS, respectively). Although mild oxidative stress resulting from cigarette smoking leads to the upregulation of the antioxidative enzymes synthesis in the lungs, high levels of ROS and RNS observed in patients with COPD overwhelm the antioxidant enzymes capacities, resulting in oxidant-mediated lung injury and cell death. In addition, depletion of antioxidative systems in the systemic circulation was consistently observed in such patients. The imbalance between the generation of ROS/RNS and antioxidant capacities -the state of "oxidative stress" -is one of the major pathophysiologic hallmarks in the development of COPD. Detrimental effects of oxidative stress include impairment of membrane functions, inactivation of membrane-bound receptors and enzymes, and increased tissue permeability. In addition, oxidative stress aggravates the inflammatory processes in the lungs, and contributes to the worsening of the protease-antiprotease imbalance. Several markers of oxidative stress, such as increases in lipid peroxidation products and reductions in glutathione peroxidase activity, have been shown to be related to the reductions in pulmonary functions. In the present article we review the current knowledge about the vicious cycle of cigarette smoking, oxidative stress, and inflammation in the pathogenesis of COPD.

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Oxidative Stress and Lung Function

Cited by 108 publications

References 55 publications

Antioxidants, oxidative stress, and pulmonary function in individuals diagnosed with asthma or COPD

Antioxidants, oxidative stress, and pulmonary function in individuals diagnosed with asthma or COPD

Molecular composition of the alveolar lining fluid in the aging lung

The role of oxidative stress in lung injury induced by cigarette smoke

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