Mikoian V D, Voevodskaia N V, Kubrina L N, Malenkova I V, Vanin A F
Biokhimiia. 1994 May;59(5):732-8.
The inhibitor of protein biosynthesis, cycloheximide (CHI) and the exogenous antioxidant, phenazan, attenuated the synthesis of nitric acid oxide (NO) in mouse liver in vivo induced by gamma-irradiation, bacterial lipopolysaccharide (LPS) or LPS+Fe(2+)-citrate treatment of experimental animals. The rate of NO synthesis was followed by accumulation of paramagnetic mononitrosyl iron complexes with the exogenous ligand--diethyldithiocarbamate (MNIC-DETC). The latter were formed as a result of NO binding to selective NO traps (DETC complexes with exogenous or endogenous Fe2+ ions) and measured by the EPR method. A conclusion is drawn that the activation of NO biosynthesis under the action of gamma-irradiation, LPS or LPS+Fe(2+)-citrate treatment was due to the induction of NO synthase synthesis inhibited by CHI. This process is initiated by active oxygen species, presumably due to the activation of the transcription factor, NFkB protein. The accumulation of active oxygen species was inhibited by the antioxidant, phenazan.
