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. 2009 Aug 6;180(10):972–981. doi: 10.1164/rccm.200902-0296OC

Figure 1.

Figure 1.

Lung injury is decreased in NADPH oxidase-1 (NOX1)-deficient but not in NADPH oxidase-2 (NOX2)-deficient mice. NOX1−/−, NOX2−/−, and wild-type (WT) mice were exposed to 100% hyperoxia for 72 hours. (A) Bronchoalveolar lavage (BAL) protein content (n ≥ 15 in each group; P = 0.68 compared with WT) and (B) BAL lactate dehydrogenase (LDH) content in NOX2−/− mice (n = 5 or 6 for each group; P = not significant [NS], NOX2−/− mice vs. WT in hyperoxia). (C) BAL protein content (n > 15 for each group; P = 0.003 compared with WT mice) and (D) BAL LDH content in NOX1−/− mice (n = 10 in each group; †P < 0.05, NOX1−/− mice vs. WT in hyperoxia). Columns and error bars represent the mean ± SEM. (E) Immunochemical detection of fibrin in paraffin-embedded lung sections. Lung sections were stained with a polyclonal anti-fibrin antibody (red) and visualized by optical microscopy. Original magnification, ×40. (F) Quantification of fibrin deposition in NOX2−/− mice and their WT control. Values represent the mean of the relative area × mean of intensity ± SEM of 10 different fields (n = 3 mice in each group); P = NS, NOX2−/− mice versus WT in hyperoxia. (G) Quantification of fibrin deposition in NOX1−/− mice and their WT control; †††P < 0.001, NOX1−/− mice versus WT in hyperoxia.