[Effect of prooxidants on nitric oxide formation in murine liver, treated with bacterial lipopolysaccharide].
Coinjection of citrate iron complex (7.5-10 mg iron/kg) with Escherichia coli lipopolysaccharide (LPS) inhibited generation of nitric oxide in the liver of mice caused by LPS-dependent synthesis of inducible NO-synthase (iNOS). Coinjection of hydroquinone, pyrogallol, or CCl4 with LPS also inhibited NO generation in the liver. Inhibition of LPS-dependent of NO synthesis in the liver by all these agents and iron can be due to their pro-oxidant effects on metabolism of this tissue. These pro-oxidants rapidly activate synthesis of low molecular weight antioxidants; LPS-dependently generated active oxygen forms in the liver of treated animals, which causes iNOS synthesis, are inactivated by the antioxidants; thus, accumulation of active oxygen species is decreased and iNOS synthesis is inhibited.
Mikoian
V D
VD
Kubrina
L N
LN
Vanin
A F
AF
D000818:Animals; D019343:Citric Acid; D004578:Electron Spin Resonance Spectroscopy; D004926:Escherichia coli / Q000378:metabolism; D005296:Ferrous Compounds / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000096:biosynthesis; D017382:Reactive Oxygen Species
D005296:Ferrous Compounds; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D019343:Citric Acid; D009569:Nitric Oxide; C016600:ferrous citrate; D019001:Nitric Oxide Synthase