AIM To evaluate the relationship between the inhibitory effect on nitric oxide production and the protective effect of melatonin
on
immunological liver injury in mice. METHODS An immunological liver injury model was induced by administration of lipopolysaccharide following injection of corynebacterium parvum into mice. Mouse hepatocytes and peritoneal macrophages were isolated and cultured. The effects of melatonin were observed by changes of alanine aminotransferase(ALT), nitric oxide(NO), molondiadehyde(MDA) and glutathione peroxidase(GSH px). RESULTS Melatonin (given at 0 1 mg and 1 0 mg·kg -1 ) inhibited the elevation of NO level( P <0 05), reduced ALT and MDA levels and partially restored GSH px activity( P <0 05～0 01) in liver damaged to mice. In contrast,
GN monomethyl L arginine remarkably reduced the elevated plasma NO ( P <0 01) while induced more pronounced liver damage. In addition, the effect of meatonin was not seen in cocultured hepatocytes and macrophages in vitro . Conclusion Melatonin was shown to be a modestly potent inhibitor or nitric oxide production, which might benefit its protective action against immunological liver injury in mice.