Abstract
Exposure to hyperoxia ( > 95% O2) is a necessary therapeutic treatment used to maintain tissue oxygenation in patients with compromised lung function and decreased pulmonary gas exchange. Hyperoxia causes increased formation of reactive oxygen species (ROS), which accumulate in the cells of the lung resulting in cell death and compromised tissue function. Recent observations have demonstrated that different lung cell types respond differently to increased oxidative stress raising many questions about the cell-type restricted response of different pulmonary cell types. This review will focus on three main aspects of chronic oxidative stress in a cell-type specific manner: the role of antioxidant defenses, DNA repair, and apoptotic signaling.
Keywords: Anti-oxidants, apoptosis, DNA damage, hyperoxia, lung, reactive oxygen species
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