| First Author | Kenyon NJ | Year | 2002 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 282 |
| Issue | 3 | Pages | L540-5 |
| PubMed ID | 11839550 | Mgi Jnum | J:75613 |
| Mgi Id | MGI:2177125 | Doi | 10.1152/ajplung.00297.2001 |
| Citation | Kenyon NJ, et al. (2002) Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice. Am J Physiol Lung Cell Mol Physiol 282(3):L540-5 |
| abstractText | 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. |
