| Literature DB >> 7682068 |
M P Sherman1, E E Aeberhard, V Z Wong, J M Griscavage, L J Ignarro.
Abstract
Since nuclear factor kappa B (NF-kappa B) is activated during many inflammatory conditions, we assessed its role in expression of the L-arginine-nitric oxide pathway by rat alveolar macrophages. Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappa B activation, was added to cultured macrophages stimulated with lipopolysaccharide (LPS) and interferon-gamma (IFN gamma). Inducible nitric oxide synthase (iNOS) activity was determined by measuring the stable nitrogen oxide end products of L-arginine oxidation: nitrite (NO2-) and nitrate (NO3-). Ten, 25 and 50 microM PDTC progressively inhibited iNOS activity by macrophages. When 50 microM PDTC was added 2 h before LPS + IFN gamma, L-arginine oxidation by macrophages was inhibited by > 99%; L-arginine oxidation was reduced by 70% if 50 microM PDTC and the stimuli were introduced together; NO2- and NO3- were not decreased significantly if 50 microM PDTC was added 6 h after LPS + IFN gamma. Cycloheximide added along with LPS + IFN gamma totally inhibits iNOS activity, while cycloheximide added 6 h after LPS + IFN gamma did not reduce NO2- and NO3- in tissue culture supernatants. These findings suggest iNOS activity in macrophages treated with LPS + IFN gamma requires NF-kappa B activation.Entities:
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Year: 1993 PMID: 7682068 DOI: 10.1006/bbrc.1993.1359
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575