Bronchopulmonary dysplasia and oxidative stress: are we closer to an understanding of the pathogenesis of BPD?

In recent years a body of data has accumulated, linking the development of bronchopulmonary dysplasia (BPD) to increased oxidative stress in the first few days after birth, since high concentrations of metabolites reflecting increased peroxidation products such as pentane, ethane, protein carbonyl, o-tyrosine, allantoin and F2-isoprostanes, as well as low levels of glutathione and sulfhydryl/total protein ratio, also reflecting increased oxidative load, have been found in the premature infants at risk of or developing BPD. Oxidative stress seems to increase lung antioxidants in some experimental models of BPD and hyperoxia affects foetal lung growth. There are similarities between inflammation and hypoxia/reoxygenation, since both activate a number of inflammatory mediators such as cytokines and adhesion molecules, some of which are found in high concentrations in tracheal aspirate fluid of infants developing BPD. Surfactant production and function are also altered by both hyperoxia and reactive oxygen species per se, making the lungs more vulnerable to injury. This new knowledge may result in new and more efficient therapeutic approaches, hopefully leading to the eradication of BPD in the near future.