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Am J Physiol Lung Cell Mol Physiol 284: L680-L687, 2003. First published January 10, 2003; doi:10.1152/ajplung.00191.2002
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Vol. 284, Issue 4, L680-L687, April 2003

Evidence for extracellular superoxide dismutase as a mediator of hemorrhage-induced lung injury

Russell P. Bowler1, John Arcaroli2, Edward Abraham2, Manisha Patel1, Ling-Yi Chang1, and James D. Crapo1

1 National Jewish Medical and Research Center, Denver 80206; and 2 Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262

Hemorrhage results in excessive production of superoxide that is associated with severe lung injury. We examined whether the superoxide dismutase (SOD) mimetic manganese(III) mesotetrakis (di-N-ethylimidazole) porphyrin (AEOL 10150) could attenuate this lung injury and whether extracellular (EC)-SOD-deficient mice would have increased hemorrhage-induced lung injury. Compared with wild-type mice, EC-SOD-deficient mice had increased lung neutrophil accumulation, a 3.9-fold increase in myeloperoxidase activity, a 1.5-fold increase in nuclear factor (NF)-kappa B activation, and a 1.5-fold increase in lipid peroxidation 1 h after hemorrhage. Pretreatment with AEOL 10150 did not attenuate neutrophil accumulation but significantly reduced NF-kappa B activation and lipid peroxidation in both wild-type and EC-SOD-deficient mice. The increase in hemorrhage-induced neutrophil accumulation in the lungs of EC-SOD-deficient mice suggests that EC-SOD might play a role in mediating neutrophil recruitment to the lung.

catalytic antioxidant; metalloporphyrin


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