Is there a role for antioxidant therapy in bronchopulmonary dysplasia?

Bronchopulmonary dysplasia (BPD) is a chronic lung disease first described in 1967 as a complication of therapy for premature infants with hyaline membrane disease, and treatment with high concentrations of oxygen was thought to be a major contributor to its development. Thus, interventions to enhance lung antioxidants to prevent the development of BPD were considered appropriate therapeutic strategies. In the last decades, advances in the acute care of premature infants has reduced the reliance on therapy with high concentrations of supplemental oxygen. However, the incidence of BPD has not changed significantly. The changing clinical context in which BPD develops begs the question of whether oxidation is important in the development of BPD and, therefore, whether designing interventions enhancing lung antioxidants is still warranted. This review presents evidence that premature infants that will develop BPD have qualitative and quantitative differences in oxidation of lipids and proteins when compared to infants that do not develop BPD. Such differences in oxidation patterns are the most obvious in the first few days of life. The emerging evidence thus supports the concept that the lung injury process leading to the development of BPD occurs within hours to days of delivery and that oxidation is a major contributor to this pathological process. Unfortunately, early attempts at delivery of antioxidants to the lung have not been successful, perhaps because of an inability to deliver antioxidants in a timely manner to the areas in the lung in which deleterious oxidations are occurring. Further research is necessary to determine both the nature and the location of the oxidative events that lead to the development of early lung injury, so that more appropriate and specific antioxidant interventions can be designed.