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Mechanisms governing the secondary burst of reactive oxygen species (ROS) and basic
pathways of cell death from hyperoxia. 1: Loss of plasma membrane integrity from lipid
peroxidation by ROS. 2: ROS damage to the mitochondria membranes and deactivation of
enzyme systems and cytochrome chain. 3: This results in the release of cytochrome c into the
cytoplasm. 4: ROS damage to the nuclear membrane and fragmentation of DNA. 5: Evolving cell
trauma from steps 1, 2, and 4 trigger the production and release of pro-inflammatory cytokines
and chemokines into the extracellular space and circulation. 6: This attracts and activates
platelets, neutrophils, and macrophages, resulting in a secondary burst of ROS from these
inflammatory cells.
Richard H Kallet, and Michael A Matthay Respir Care
2013;58:123-141
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