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l ‐Arginine depletion by arginase reduces nitric oxide production in endotoxic shock: an electron paramagnetic resonance study
Author(s) -
Bune A.J.,
Shergill J.K.,
Cammack R.,
Cook H.T.
Publication year - 1995
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 - 10.1016/0014-5793(95)00495-u
Subject(s) - nitric oxide , arginase , chemistry , arginine , lipopolysaccharide , electron paramagnetic resonance , nitrite , extracellular , in vivo , septic shock , biochemistry , endocrinology , biophysics , medicine , nuclear magnetic resonance , biology , sepsis , amino acid , physics , microbiology and biotechnology , organic chemistry , nitrate
Nitric oxide (NO) synthesis was measured in the liver, lung, spleen and kidney of lipopolysaccharide‐treated male rats using the nitric oxide spin trap, iron (II)‐diethyldithiocarbamate (FeDETC 2 ). Nitric oxide formation in vivo was determined by the increase in intensity of the characteristic triplet hyperfine EPR spectrum of [NO‐FeDETC 2 ]. Intravenous bovine liver arginase, at a dose which completely depleted circulating arginine, significantly reduced the formation of nitric oxide in these tissues. The general decrease in NO levels was confirmed by the decrease in plasma nitrite levels. These results directly demonstrate that NO formation in endotoxic shock depends on extracellular arginine; depletion of plasma arginine may be a useful therapeutic strategy.