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(The FASEB Journal. 2002;16:1713-1720.)
© 2002 FASEB

In vivo lipid-derived free radical formation by NADPH oxidase in acute lung injury induced by lipopolysaccharide: a model for ARDS

KEIZO SATO1, MARIA B. KADIISKA, ANDREW J. GHIO*, JEAN CORBETT, YANG C. FANN, STEVEN M. HOLLAND§, RONALD G. THURMAN{dagger},2 and RONALD P. MASON

Free Radical Metabolite Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA;
* National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, North Carolina, USA;
§ Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA; and
{dagger} Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, and Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina, USA

1Correspondence: Free Radical Metabolite Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, P.O. Box. 12233, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA. E-mail: sato{at}niehs.nih.gov

Intratracheal instillation of lipopolysaccharide (LPS) activates alveolar macrophages and infiltration of neutrophils, causing lung injury/acute respiratory distress syndrome. Free radicals are a special focus as the final causative molecules in the pathogenesis of lung injury caused by LPS. Although in vitro investigation has demonstrated radical generation after exposure of cells to LPS, in vivo evidence is lacking. Using electron spin resonance (ESR) and the spin trap {alpha}-(4-pyridyl-1-oxide)-N-tert-butylnitrone (POBN), we investigated in vivo free radical production by rats treated with intratracheal instillation of LPS. ESR spectroscopy of lipid extract from lungs exposed to LPS for 6 h gave a spectrum consistent with that of a POBN/carbon-centered radical adduct (aN=14.94±0.07 G and aßH=2.42±0.06 G) tentatively assigned as a product of lipid peroxidation. To further investigate the mechanism of LPS-initiated free radical generation, rats were pretreated with the phagocytic toxicant GdCl3, which significantly decreased the production of radical adducts with a corresponding decrease in neutrophil infiltration. NADPH oxidase knockout mice completely blocked phagocyte-mediated, ESR-detectable radical production in this model of acute lung injury. Rats treated intratracheally with LPS generate lipid-derived free radicals via activation of NADPH oxidase.—Sato, K., Kadiiska, M. B., Ghio, A. J., Corbett, J., Fann, Y. C., Holland, S. M., Thurman, R. G., Mason, R. P. In vivo lipid-derived free radical formation by NADPH oxidase in acute lung injury induced by lipopolysaccharide: a model for ARDS.


Key Words: spin trapping • knockout mice • GdCl3




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