Abstract
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, N G - 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 Ca 2+ ions into NO-producing cells through Fe 2+-induced cell membrane lesions.
Published Version
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