Antioxidants and oxidations in bronchopulmonary dysplasia: there are no easy answers

Abstract

Bronchopulmonary dysplasia (BPD) was first described in 1967 as a complication of prematurity, and the pathophysiology was thought to include oxygen toxicity and barotrauma in premature infants with hyaline membrane disease. In this form of BPD, the lung pathology primarily consisted of an injured, fibrotic lung. Intense research efforts have been directed toward determining mechanisms for the development of BPD and interventions to prevent or ameliorate its severity. Since then, surfactant administration and other improvements in neonatal intensive care have improved the acute condition of premature infants. It was fair to speculate that the incidence of BPD would fall. Unfortunately, chronic lung disease still develops in extremely premature infants that do not have significant ventilatory or supplemental oxygen needs in the acute course of prematurity. This form of new BPD is less fibrotic than its earlier counterpart, and there is a significant component of delayed alveolar development and perhaps permanent alveolar underdevelopment.1,2 Currently, the mechanisms for the development in the new form of BPD have not been fully elucidated and the contribution of oxygen toxicity is debatable. However, it is plausible that even low concentrations of supplemental oxygen in premature patients with developmentally poorly prepared antioxidant defense mechanisms may generate significant oxidant stresses and lung injury secondary to oxidation of specific macromolecules. In addition, inflammatory cell accumulation and activation in the lung may also generate oxidants and oxidant stresses that also oxidize macromolecules.