Bronchial asthma is an inflammatory disorder characterized by recruitment and activation of various inflammatory cells including eosinophils and T cells in the airway mucosa. Oxygen radicals are produced by inflammatory cells in the airways and/or inhaled directly from environmental air. There is ample evidence that oxygen radical production is increased in asthma and is closely related to the pathogenesis and that exogenous oxidants such as cigarette smoke and ozone directly cause asthma exacerbation. The mechanism by which oxygen radicals cause asthma pathology is oxidation or nitration of proteins, lipids, or DNA to cause dysfunction of these molecules. In addition, physiological antioxidant system, which is equipped to protect host from detrimental oxidants, is impaired in asthma, possibly because of inflammation. Thus, the imbalance between oxidant and antioxidant that is called oxidant stress is critical in asthma pathogenesis. Elegant technique to measure oxygen radicals and the footprints of oxidant stress in patients with asthma have been developed and give an important clue to evaluate possible involvement of oxygen radicals in individual pathophysiology. Therapeutic interventions that reduce oxidant stress and enhance antioxidant defense may be useful in the treatment of asthma.
Keywords: superoxide, nitric oxide, peroxynitrite, hydrogen peroxide, nitrotyrosine airway inflammation, antioxidant, eosinophils
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