ABSTRACT

The pathogenesis of bronchopulmonary dysplasia (BPD) is complex and may depend on the nature of the injury, mechanisms of response, or the infant’s inability to respond appropriately to the injury process. Although the etiology is multifactorial in nature, prolonged exposure of the lung to supraphysiologic oxygen concentrations does appear to be critically important (1). Under normal conditions, a delicate balance exists between the production of reactive oxygen species (ROS) and the antioxidant defenses that protect cells in vivo. Increased generation of ROS can occur secondary to hyperoxia, reperfusion, or inflammation (2). Alternatively, ROS can increase because of an inability to quench production because of inadequate antioxidant defenses.