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Am J Physiol Lung Cell Mol Physiol (January 10, 2003). doi:10.1152/ajplung.00191.2002
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Submitted on June 18, 2002
Accepted on December 16, 2002

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 Department of Medicine, National Jewish Medical and Research Center, Denver, Co, USA
2 Department of Medicine, University of Colorado Health Sciences Center, Denver, Co, USA

* To whom correspondence should be addressed. E-mail: BowlerR{at}njc.org.

Hemorrhage results in excessive production of superoxide that is associated with severe lung injury. We examined whether the superoxide dismutase (SOD) mimetic manganese (III) meso-tetrakis (di-N-ethylimidazole) porphyrin (AEOL 10150) could attenuate this lung injury and whether extracellular SOD (EC-SOD) deficient mice would have increased hemorrhage-induced lung injury. Compared to wildtype 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-k B activation and a 1.5-fold increase in lipid peroxidation one hour after hemorrhage. Pretreatment with AEOL 10150 did not attenuate neutrophil accumulation, but significantly reduced NF-kB activation and lipid peroxidation in both wildtype and EC-SOD deficient mice. The increase in hemorrhage-induced neutrophil accumulation in the lungs of EC-SOD deficient mice suggest that EC-SOD might play a role in mediating neutrophil recruitment to the lung.




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