Extracellular Superoxide Dismutase Attenuates Lung Injury after Hemorrhage

Reperfusion of the lung after hemorrhage generates free radicals such as superoxide (O(2)(.)) that may injure the lung; however, the relative importance of intracellular versus extracellular free radicals is unclear. The superoxide dismutases (SOD) are the primary enzymatic method to reduce superoxi...

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Published in:American journal of respiratory and critical care medicine 2001-07, Vol.164 (2), p.290-294
Main Authors: BOWLER, RUSSELL P, ARCAROLI, JOHN, CRAPO, JAMES D, ROSS, ARON, SLOT, JAN W, ABRAHAM, EDWARD
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Free Radical Scavengers - therapeutic use
Hemorrhage - complications
Lung Diseases - drug therapy
Lung Diseases - etiology
Medical sciences
Mice
Pneumology
Respiratory system : syndromes and miscellaneous diseases
Superoxide Dismutase - therapeutic use
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Summary:Reperfusion of the lung after hemorrhage generates free radicals such as superoxide (O(2)(.)) that may injure the lung; however, the relative importance of intracellular versus extracellular free radicals is unclear. The superoxide dismutases (SOD) are the primary enzymatic method to reduce superoxide. We examined whether lung-specific overexpression of extracellular superoxide dismutase (EC-SOD) would attenuate hemorrhage-induced lung injury. Wild-type mice and mice overexpressing the human EC-SOD gene with a lung-specific promoter were hemorrhaged by removing 30% of blood volume. After hemorrhage, the lung wet to dry weight ratios increased from 5.4 +/- 0.11 in unmanipulated control mice to 6.3 +/- 0.16 in wild-type mice, but to only 5.60 +/- 0.17 in the EC-SOD transgenic mice (p < 0.05 compared with hemorrhaged wild-type). Hemorrhage-induced lipid peroxidation, as assessed by lung F(2) isoprostanes, was lower in the EC-SOD transgenic mice (3.4 +/- 0.3 microg/lung) compared with wild-type mice (1.9 +/- 0.2 microg/lung; p < 0.05). Compared with wild-type, EC-SOD transgenic mice had attenuated the hemorrhage-induced increase in both pulmonary nuclear factor kappa B (NK-kappaB) activation (relative absorbance 1.1 +/- 0.2 for EC-SOD transgenic versus 2.5 +/- 0.1 for wild-type; p < 0.05) and myeloperoxidase activity (5.1 +/- 0.87 units/g for EC-SOD transgenic versus 11.3 +/- 1.8 units/g for wild-type; p < 0.01). Thus, overexpression of pulmonary EC-SOD in the mouse lung attenuates lung injury after hemorrhage.
ISSN:1073-449X
1535-4970
DOI:10.1164/ajrccm.164.2.2011054