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Am J Physiol Lung Cell Mol Physiol (October 19, 2001). doi:10.1152/ajplung.00297.2001
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Articles in PresS, published online ahead of print October 18, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00297.2001
Submitted on August 1, 2001
Accepted on October 16, 2001

Susceptibility to Ozone-Induced Acute Lung Injury in iNOS-Deficient Mice

Nicholas J Kenyon1, Albert van der Vliet1, Bettina C Schock1, Tatsuya Okamoto1, Gabrielle M McGrew1, and Jerold A Last1*

1 Pulmonary/Critical Care Medicine, University of California, Davis, CA, USA

* To whom correspondence should be addressed. E-mail: jalast{at}ucdavis.edu.

Mice deficient in iNOS (C57Bl/6Ai-[KO]NOS2 N5) or wild type C57Bl/6 mice were exposed to 1 ppm of ozone 8 hours per night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, MIP-2, MMP-9, and 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 NO.




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