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The Journal of Immunology, Vol 146, Issue 4 1294-1302, Copyright © 1991 by American Association of Immunologists
ARTICLES |
DL Granger, JB Hibbs Jr and LM Broadnax
Division of Infectious Diseases, Duke University School of Medicine, Durham, NC 27710.
Murine macrophage oxidation of L-arginine guanidino nitrogen to nitrite/nitrate yields an intermediate effector, possibly nitric oxide, with antimicrobial activity. Total body nitrogen oxidation metabolism (NOM) was measured in vivo by determining the urinary nitrate excretion of mice ingesting a chemically defined nitrite/nitrate-free diet. As reported previously, mycobacterial infection with bacillus Calmette- Guerin led to a large increase in urinary nitrate excretion. This increase was temporally related to macrophage activation in vivo. The substrate for macrophage nitrogen oxidation metabolism in vitro, L- arginine, was deleted from the diet without ameliorating the urinary nitrate excretion response induced by BCG. This suggested that L- arginine was synthesized endogenously because there are no other known natural substrates for NOM. A competitive inhibitor of NOM, the L- arginine analog, NG-monomethyl-L-arginine was fed to mice in their drinking water. NG-monomethyl-L-arginine ingestion blocked both basal and bacillus Calmette-Guerin-induced urinary nitrate excretion over a 2- 4 week time span. These experimental conditions should prove useful for further investigation on the role of macrophage NOM in host defense against intracellular microorganisms.
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