Abstract
Purpose: Sodium nitrite, a food additive that is used as a color fixative and preservative for meats and fish, has been reported to have adverse health effects due to increased oxidative stress that could be harmful to different organs including the liver. Meanwhile, silymarin protects against hepatotoxicity caused by a variety of agents, on account of its antioxidative and anti-inflammatory effects. We therefore examined the impact of dietary silymarin on sodium nitrite-induced liver damage in rats. Methods: Fifty adult male Sprague-Dawley rats received 80 mg/kg sodium nitrite in the presence or absence of silymarin (10 and 25 mg/kg). Hepatic proinflammatory cytokines (TNF-alpha and IL-1 beta), hepatic fibrosis marker (MCP-1 and TGF-beta 1), mitochondrial activity marker (cytochrome C oxidase) and c-reactive protein (CRP) levels were measured. Hepatic apoptosis was assessed through determination of caspase-3 activity and DNA fragmentation. Results: We found that oral sodium nitrite enhanced oxidative stress with subsequent increases in TNF-alpha (2-fold), IL-1 beta (4-fold), MCP-1 (4-fold), TGF-beta 1 (3-fold) and CRP (4-fold). In addition, sodium nitrite brings about reduced cytochrome C oxidase and enhanced caspase-3 activity and DNA fragmentation. Daily treatment with silymarin markedly ameliorated all these effects. Conclusions: Silymarin ameliorated the impairment of hepatic function in rats that had ingested sodium nitrite. Silymarn possesses antioxidant, anti-inflammatory, antifibrotic and anti-apoptotic effects.