Role of free nitrogen and oxygen radicals in the pathogenesis of lipopolysaccharide-induced endotoxemia.

We studied molecular mechanisms of changes in oxidative metabolism under conditions of experimental lipopolysaccharide-induced endotoxemia. Generation of reactive nitrogen and oxygen species in mice increased 18 h after treatment with lipopolysaccharide. These changes contributed to inactivation of enzymes and enzyme complexes (ribonucleotide reductase, NADH-ubiquinone oxidoreductase, and cytochrome c oxidase), dysfunction of the mitochondrial electron transport chain, and development of oxidative stress. Plaferon LB protected mice from the toxic effect of lipopolysaccharide.