Premium
Iron attenuates nitric oxide level and iNOS expression in endotoxin‐treated mice
Author(s) -
Komarov Andrei M,
Mattson David L,
Mak I.Tong,
Weglicki William B
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00181-1
Subject(s) - nitric oxide , chemistry , nitric oxide synthase , biochemistry , endocrinology , medicine , biology , organic chemistry
The effect of exogenous Fe‐citrate complex (Fe doses of 120 and 240 μmol/kg) on nitric oxide (NO) production in vivo has been studied in blood and liver tissue of endotoxin‐treated mice. Fe‐citrate complex was administered to mice subcutaneously at the same time with intravenous injection of Escherichia coli lipopolysaccharide (LPS). Iron‐dependent decrease in NO − 2 /NO − 3 and nitrosyl hemoglobin levels in blood of animals was detected at 6 h after LPS administration, suggesting systemic attenuation of NO generation. NO production in the liver tissue of LPS‐treated mice was decreased after Fe administration judging from the amount of mononitrosyl‐iron complexes formed in the tissue by diethyldithiocarbamate. The iNOS protein determination in the liver tissue of LPS‐treated mice demonstrated iron‐dependent inhibition of iNOS expression. We have found previously that exogenous iron does not affect systemic NO level when it is given at 6 h after LPS injection, i.e. after iNOS expression. This is a first report demonstrating iron‐dependent iNOS down‐regulation in endotoxin‐treated mice.