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Am J Physiol Lung Cell Mol Physiol 282: L540-L545, 2002. First published October 19, 2001; doi:10.1152/ajplung.00297.2001
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Vol. 282, Issue 3, L540-L545, March 2002

Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice

Nicholas J. Kenyon, Albert van der Vliet, Bettina C. Schock, Tatsuya Okamoto, Gabrielle M. McGrew, and Jerold A. Last

Pulmonary/Critical Care Medicine, School of Medicine, University of California, Davis, California 95616-8723

Mice deficient in inducible nitric oxide synthase (iNOS; C57Bl/6Ai-[KO]NOS2 N5) or wild-type C57Bl/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclear leukocytes. The iNOS knockout mice showed significantly greater levels of lung injury by all of these criteria than did the wild-type mice. We conclude that iNOS knockout mice are more susceptible to acute lung damage induced by exposure to ozone than are wild-type C57Bl/6 mice and that protein nitration is associated with the degree of inflammation and not dependent on iNOS-derived nitric oxide.

nitrotyrosine; nitric oxide; inflammation; matrix metalloproteinase-9; macrophage inflammatory protein-2


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