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

Nicholas Kenyon, Albert Van Der Vliet, Bettina C. Schock, Tatsuya Okamoto, Gabrielle M. McGrew, Jerold A Last

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


Mice deficient in inducible nitric oxide synthase (iNOS; C57B1/6Ai-[KO]NOS2 N5) or wild-type C57B1/6 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 C57B1/6 mice and that protein nitration is associated with the degree of inflammation and not dependent on iNOS-derived nitric oxide.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number3 26-3
StatePublished - 2002


  • Inflammation
  • Macrophage inflammatory protein-2
  • Matrix metalloproteinase-9
  • Nitric oxide
  • Nitrotyrosine

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology


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