Background: Prolonged exposure to high oxygen concentrations in premature infants, although lifesaving, can induce lung oxidative stress and increase the risk of developing BPD, a form of chronic lung disease. The lung alveolar epithelium is damaged by sustained hyperoxia, causing oxidative stress and alveolar simplification; however, it is unclear what duration of exposure to hyperoxia negatively impacts cellular function.
Methods: Here we investigated the role of a very short exposure to hyperoxia (95% O, 5% CO) on mitochondrial function in cultured mouse lung epithelial cells and neonatal mice.