NSO ameliorates sodium nitrite-induced nephrotoxicity through blocking oxidative stress, attenuation of fibrosis/inflammation, restoration of glycogen level, amelioration of cytochrome C oxidase, and inhibition of apoptosis.

Context: Exposure to high levels of nitrites for a prolonged time have adverse health effects on several organs especially the liver due to oxidative properties. Meanwhile, cod liver oil has been reported to ameliorate organ dysfunction in animal models that involve oxidative stress. Objective: Examine the impact of dietary cod liver oil on sodium nitrite-induced liver damage. Materials and methods: Thirty-two adult male Sprague-Dawely rats were daily treated with sodium nitrite (80 mg/kg) in presence or absence of cod liver oil (5 ml/kg). Morphological changes were assessed in liver sections. Oxidative stress and antioxidant markers were measured in serum and liver homogenates. Liver samples were used for measurements of MCP-1, DNA fragmentation and mitochondrial function. Results: The hepatoprotective effect of cod liver oil was proved by significant reduction of elevated liver enzymes and normal appearance of hepatocytes. Cod liver oil significantly reduced hepatic malondialdehyde, hydrogen peroxide and superoxide anion (224.3 AE 18.9 nmol/g, 59.3 AE 5.1 and 62.5 AE 5.1 mmol/g, respectively) compared with sodium nitrite (332.5 AE 25.5 nmol/g, 83.1 AE 8.1 and 93.9 AE 6.5 mmol/g, respectively). Cod liver oil restored hepatic cytochrome c oxidase activity after 38% reduction by sodium nitrite. Furthermore, cod liver oil significantly reduced hepatic MCP-1 (79.8 pg/mg) and DNA fragmentation (13.8%) compared with sodium nitrite (168.7 pg/mg and 41.3%, respectively). Discussion and conclusion: Cod liver oil ameliorates sodium nitrite induced hepatic impairment through several mechanisms including attenuation of oxidative stress, blocking MCP-1, reactivation of mitochondrial function and reduction of DNA fragmentation.

No abstract

No abstract

No abstract