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

نویسندگان

  • Nicholas J Kenyon
  • Albert van der Vliet
  • Bettina C Schock
  • Tatsuya Okamoto
  • Gabrielle M McGrew
  • Jerold A Last
چکیده

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.

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عنوان ژورنال:
  • American journal of physiology. Lung cellular and molecular physiology

دوره 282 3  شماره 

صفحات  -

تاریخ انتشار 2002