Iron potentiates bacterial lipopolysaccharide-induced nitric oxide formation in animal organs.
Administration of an Fe(2+)-citrate complex to mongrel mice pretreated with lipopolysaccharide (LPS) from Salmonella typhosa increased LPS-induced NO formation in vivo in the liver, intestine, lung, heart, kidney and spleen by 10-20-fold. This process was monitored by the intensity of the EPR signal due to mononitrosyl iron complex (MNIC) formation with exogenous diethyldithiocarbamate (DETC) recorded in the tissues. The NO synthase inhibitor, NG-nitro-L-arginine, prevented this complex formation in the liver of mice treated with both LPS and Fe(2+)-citrate complex. Thus, administration of LPS and Fe(2+)-citrate complex to mice induced NO biosynthesis in this tissue via an L-arginine-dependent pathway, presumably by facilitating the entry of Ca2+ ions into NO-producing cells through Fe(2+)-induced cell membrane lesions.
Kubrina
L N
LN
Institute of Chemical Physics, Russian Academy of Sciences, Moscow.
Mikoyan
V D
VD
Mordvintcev
P I
PI
Vanin
A F
AF
D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors; D000818:Animals; D004050:Ditiocarb / Q000008:administration & dosage; D004578:Electron Spin Resonance Spectroscopy; D005290:Ferric Compounds; D007501:Iron / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000008:administration & dosage*; D008099:Liver / Q000378:metabolism; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase
D005290:Ferric Compounds; D008070:Lipopolysaccharides; D009569:Nitric Oxide; C025314:ferric citrate; D004050:Ditiocarb; D007501:Iron; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases