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

Abstract

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)-kappaB 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-kappaB 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.

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@article{Bowler2003EvidenceFE, title={Evidence for extracellular superoxide dismutase as a mediator of hemorrhage-induced lung injury.}, author={Russell P Bowler and John J. Arcaroli and Edward H. Abraham and Manisha Patel and Ling Chang and James D. Crapo}, journal={American journal of physiology. Lung cellular and molecular physiology}, year={2003}, volume={284 4}, pages={L680-7} }