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.