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ABSTRACT: Rationale
Hyperoxia-induced acute lung injury has been used for many years as a model of oxidative stress mimicking clinical acute lung injury and the acute respiratory distress syndrome. Excess quantities of reactive oxygen species (ROS) are responsible for oxidative stress-induced lung injury. ROS are produced by mitochondrial chain transport, but also by NADPH oxidase (NOX) family members. Although NOX1 and NOX2 are expressed in the lungs, their precise function has not been determined until now.Objectives
To determine whether NOX1 and NOX2 contribute in vivo to hyperoxia-induced acute lung injury.Methods
Wild-type and NOX1- and NOX2-deficient mice, as well as primary lung epithelial and endothelial cells, were exposed to room air or 100% O(2) for 72 hours.Me
SUBMITTER: Carnesecchi S
PROVIDER: S-EPMC2778156 | biostudies-literature | 2009 Nov
REPOSITORIES: biostudies-literature