Role of nitric oxide in immunological liver damage in mice

Abstract The role of nitric oxide (NO) in immunological liver injury in mice was studied. Moderate increases in plasma NO levels and liver damage were seen after the injection of either Bacillus Calmette-Guerin (BCG) or lipopolysaccharide (LPS) alone in mice. Administration of LPS following BCG injection resulted in a remarkable elevation of the plasma NO level and severe liver damage. The elevation of the NO level and the liver damage induced by BCG or BCG + LPS were not affected by the administration of l -arginine. The BCG-induced increase of plasma NO was inhibited by N G -monomethyl-L-arginine (NMA) treatment without effect on the elevated plasma glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) levels. The BCG + LPS-induced elevation of plasma GPT and GOT levels was more pronounced after NO production was inhibited by NMA treatment. The action of NMA mentioned above was partially reversed by the simultaneous administration of l -arginine. These findings suggest that NO plays a protective role against liver injury induced by BCG + LPS in mice.