Evidence of oxidative stress in asthma and COPD: potential inhibitory effect of theophylline

Tsukagoshi, Hideo; Shimizu, Yasuo; Iwamae, Shigenori; Hisada, Takeshi; Ishizuka, Tamotsu; Iizuka, Kunihiko; Dobashi, Kunio; Mori, Masatomo

doi:10.1053/rmed.2000.0785

Cited by 46 publications

(35 citation statements)

References 23 publications

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“…In addition, these LPO products negatively correlate with the lung function marker forced expiratory volume in one second (FEV1), suggesting that lipid peroxidation plays an important role in the decline of lung function [28]. In the plasma and lung lavages of healthy smokers the levels of LPO products are also increased.…”

Section: Lipid Peroxidation Productsmentioning

confidence: 99%

Oxidant metabolism in chronic obstructive pulmonary disease

Boots

Haenen

Bast

2003

European Respiratory Journal

105

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The development and progression of chronic obstructive pulmonary disease (COPD) have been associated with increased oxidative stress or reduced antioxidant resources. Several indicators of oxidative stress, such as hydrogen peroxide exhalation, lipid peroxidation products and degraded proteins, are indeed elevated in COPD patients. As a result, the antioxidant capacity decreases in COPD patients.The fall in antioxidant capacity of blood from COPD patients should not only be regarded as a reflection of the occurrence of oxidative stress but also as evidence that oxidative stress spreads out to the circulation and can therefore generate a systemic effect.COPD is linked to weight loss and in particular to loss in fat-free mass by skeletal muscle wasting. This systemic effect can be mediated by both oxidative stress and oxidative stress-mediated processes like apoptosis and inflammation. Furthermore, COPD is a predisposition for lung cancer through several mechanisms including oxidative stress and oxidative stress-mediated processes such as inflammation and disruption of genomic integrity.Current therapeutic interventions against the far-reaching consequences of the systemic oxidative stress in chronic obstructive pulmonary disease are not yet optimised. A diet designed to reduce chronic metabolic stress might form an effective therapeutic strategy in chronic obstructive pulmonary disease.

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Section: Lipid Peroxidation Productsmentioning

confidence: 99%

Oxidant metabolism in chronic obstructive pulmonary disease

Boots

Haenen

Bast

2003

European Respiratory Journal

105

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“…This may undergo oxidation to produce the end product of lipid peroxidation such as 4-HNE [25,28]. The levels of plasma lipid peroxides (TBARS) have been shown to be elevated in asthma, and negatively correlated with the forced expiratory volume in one second (FEV 1 ) suggesting that increased oxidative stress occurs in patients with asthma [99,100]. Further studies are needed to define the source, significance and specificity of these peroxidation products in patients with asthma.…”

Section: Role Of Epo-derived Rosmentioning

confidence: 99%

Oxidative Stress and Gene Transcription in Asthma and Chronic Obstructive Pulmonary Disease: Antioxidant Therapeutic Targets

Rahman¹

2002

CDTIA

102

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Inflammatory lung diseases such as asthma and Chronic Obstructive Pulmonary Disease (COPD) are characterised by systemic and local chronic inflammation and oxidative stress. The sources of the increased oxidative stress in patients with asthma and COPD derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and structural cells of the airways. Increased levels of ROS produced in the airways are reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with asthma and COPD. ROS, either directly or via the formation of lipid peroxidation products such as acrolein, 4-hydroxy-2-nonenal and F 2 -isoprostanes, may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38, phosphoinositide 3 (PI-3)-kinase/PI-3K-activated serine-threonine kinase Akt) and redox sensitive transcription factors such as NF-κB and AP-1. Recent data have also indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Furthermore, oxidative stress may alter the balance between gene expression of pro-inflammatory mediators and antioxidant enzymes in favor of inflammatory mediators in the lung. Thus, the presence of oxidative stress may have important consequences for the pathogenesis of asthma and COPD. Identification of genes that predispose to the development of asthma and COPD may identify novel therapeutic targets. Future work is directed to understand the molecular mechanisms of antioxidants on ROS-mediated cell signaling pathways and inhibition of inflammatory response that would provide information for the development of novel antioxidant therapeutic targets in asthma and COPD. Effective wide spectrum antioxidant therapy that has good bioavailability and potency is urgently needed to control the localised oxidative and inflammatory processes that occur in the pathogenesis of asthma and COPD. In addition, development of such novel antioxidant compounds would be therapeutically useful in monitoring the oxidative and inflammatory biomarkers in the progression/severity of asthma and COPD.

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“…There is increasingly persuasive evidence to suggest that increased oxidative stress, the imbalance between protective antioxidants and free radical activity, may be involved in the pathophysiology of COPD [7,22]. Sources for these oxidants are for example, cigarette smoke, and activated inflammatory cells.…”

Section: Discussionmentioning

confidence: 99%