Demonstrates that hydroxyl radicals drive phagocyte-dependent acute lung injury in animal models, suggesting targeted antioxidant interventions can protect pulmonary tissue.
Studies in experimental animals suggest that oxygen-derived free radicals are playing an important pathophysiologic role in cell and tissue damage. Systemic activation of the complement system or deposition of immune complexes in alveolar spaces results in activation of phagocyte-dependent NADPH oxidase and subsequent release of oxygen radicals that cause acute lung injury and appearance of lipid peroxidation products in lung tissue and plasma. Since pretreatment of experimental animals with catalase, iron chelators or scavengers of hydroxyl radical results in protection from pulmonary damage, it is assumed that the hydroxyl radical is the most likely mediator of phagocyte-dependent acute lung injury.
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Ward et al. (2009) studied this question.
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