Uncontrolled excessive immune reaction may cause tissue damage and destruction by acute or chronic inflammations. Reactive oxygen species generated from active neutrophils and macrophages are known as principal causative factors in inflammatory
tissue
damage. In the present study, role of nitric oxide generation in tissue injury was examined in immune complex-mediated experimental glomerulonephritis. When concanavalin A and its antiserum were injected into rat, urinary protein excretion during
24h
was increased as a parameter of function impairment. Excretion of nitrite and nitrate, stable oxidation products of nitric oxide, were elevated by the administration of immune complex indicating induction of nitric oxide synthase. Protein
excretion
in
24h urine was diminished along with decreased nitrite/nitrate generation by addition of N-methyl-L-arginine, a competitive inhibitor of nitric oxide synthase. This protective effect of N-methyl-L-arginine was abolished by excess L-arginine not by
D-arginine. Concentrations of lipid hydroperoxide, an intermediate substance in lipid peroxidation, in renal tissue were increased by elevated nitric oxide synthase activity(indicate by high nitrite/nitrate excretion) and decreased by depressed
nitric
oxide synthase activity. These results suggested that nitric oxide could play an role in tissue damage in immune complex-mediated inflammations.
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