Dimethylnitrosamine (DMN) is a potent hepatotoxic, carcinogenic and mutagenic compound. It induces massive liver cell necrosis and death in experimental animals. Several drugs have been tested in the past for their protective behavior against DMN toxicity. However, it is for the first time that therapeutic intervention of ZnONPs (zinc oxide nanoparticles) has been studied against its toxicity. Present results show that a post treatment of ZnONPs (50 mg/kg) to DMN (2 μl/100 g body weight) treated rats reduces lipid peroxidation, oxidative stress and fibrosis in the liver. It diminishes serum ALT (alanine transaminases), AST (aspartate transaminases) and LDH (lactate dehydrogenase) showing improvement in liver function. Reduced values of proinflammatory cytokines viz. TNF-α and IL-12 also support its protective effects. Histopathological observations also indicate improvement in liver cell morphology. It is postulated that ZnONPs offer protection through selective toxicity to proliferating tissue including adenomatous islands formed in the liver. Zinc metallothionein (Zn-MT) induced by ZnONPs may also contribute in the amelioration of DMN induced toxic effects. Diminution of oxidative stress by ZnONPs remains to be the key mechanism involved in its protective effects. However, toxicity of ZnONPs in the liver needs to be monitored simultaneously.
Keywords: Dimethylnitrosamine; Fibrosis; Hepatotoxicity; IL-12; Oxidative stress; TNF-α; Zinc oxide nanoparticles.
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