Oxidant--antioxidant imbalance in asthma: scientific evidence, epidemiological data and possible therapeutic options

Prevalence of asthma has increased considerably in recent decades throughout the world especially in developed countries. Airway inflammation is thought to be prime cause for repeated episodes of airway obstruction in asthmatics. Several studies have shown that reactive oxygen species (ROS) play a k...

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Veröffentlicht in:Therapeutic advances in respiratory disease 2008-08, Vol.2 (4), p.215
Hauptverfasser: Nadeem, Ahmed, Masood, Anbrin, Siddiqui, Nahid
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Sprache:eng
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Zusammenfassung:Prevalence of asthma has increased considerably in recent decades throughout the world especially in developed countries. Airway inflammation is thought to be prime cause for repeated episodes of airway obstruction in asthmatics. Several studies have shown that reactive oxygen species (ROS) play a key role in initiation as well as amplification of inflammation in asthmatic airways. Excessive ROS production in asthma leads to alteration in key enzymatic as well as nonenzymatic antioxidants such as glutathione, vitamins C and E, beta-carotene, uric acid, thioredoxin, superoxide dismutases, catalase, and glutathione peroxidases leading to oxidant-antioxidant imbalance in airways. Oxidant-antioxidant imbalance leads to pathophysiological effects associated with asthma such as vascular permeability, mucus hypersecretion, smooth muscle contraction, and epithelial shedding. Epidemiological data also support the scientific evidence of oxidant-antioxidant imbalance in asthmatics. Therefore, the supplementation of antioxidants to boost the endogenous antioxidants or scavenge excessive ROS production could be utilized to dampen/prevent the inflammatory response in asthma by restoring oxidant-antioxidant balance. This review summarizes the scientific and epidemiological evidence linking asthma with oxidant-antioxidant imbalance and possible antioxidant strategies that can be used therapeutically for better management of asthma.
ISSN:1753-4658
DOI:10.1177/1753465808094971