2006
DOI: 10.1096/fasebj.20.4.a725-d
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Sequential formation of reactive oxygen species by mitochondria and NAD(P)H oxidase in lung endothelial cells during hyperoxia

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“…However, ROS can also damage cellular structures through “oxidative stress,” resulting in inflammation and cell death ( 21 , 22 ). ROS concentrations in pulmonary endothelial cells increase exponentially with hyperoxia exposure, initiating a profound inflammatory response, endothelial cell injury, capillary leak and edema formation, culminating in cell death ( 23 ). Both severe hyperoxia and longer durations of MV exacerbate severe pro-inflammatory pulmonary responses in mechanically ventilated mice ( 24 ).…”
mentioning
confidence: 99%
“…However, ROS can also damage cellular structures through “oxidative stress,” resulting in inflammation and cell death ( 21 , 22 ). ROS concentrations in pulmonary endothelial cells increase exponentially with hyperoxia exposure, initiating a profound inflammatory response, endothelial cell injury, capillary leak and edema formation, culminating in cell death ( 23 ). Both severe hyperoxia and longer durations of MV exacerbate severe pro-inflammatory pulmonary responses in mechanically ventilated mice ( 24 ).…”
mentioning
confidence: 99%