Oxygen radicals

Abstract

Oxygen radicals such as O2- and H2O2 induce bronchoconstriction and airway hyperresponsiveness in animal models. Eosinophil peroxidase (EPO)+H2O2+halide system cause damage of respiratory epithelium, in vitro. Damage to airway epithelium may decrease the release of epithelium-derived relaxing factor (EpDRF) and trigger an axon reflex with the release of neuropeptides, such as substance P. Activated human eosinophils can release various inflammatory mediators, such as oxygen radicals, eosinophil granule proteins and leukotrienes, in vitro. The degree of the damage of the bronchial epithelium and the number of infiltrated and activated eosinophils in the bronchial epithelium correlate with the level of airway responsiveness in bronchial asthma patients. Therefore, eosinophil-derived oxygen radicals may contribute to the epitherial damage and enhance airway hyper-responsiveness in bronchial asthma.