Curcumin Ameliorates The Hepatoxic Effects of Nitrites: A biochemical Experimental Study

Abstract

Background and aim: Sodium Nitrate is widely used all over the world and subjects are at risk of their toxic effects. Its use is inevitable and thus proper prophylaxis against its toxic effects is crucial. Curcumin is a medicinal plant with different uses, and it is suggested to produce prophylactic actions against nitrate toxicity. Here we tested the effects of acute oral exposure of NaNO₂ and potential ameliorative effects of pre-treatment by curcumin.

Methodology: An experimental study was designed by four groups of animals (each 10 rats). The first was the control group (animals received orally, 2ml/kg, body weight of olive oil (vehicle) daily); the second is the NaNO₂ where animals received 2ml/kg, body weight of olive oil and a single dose of NaNO₂ (60mg/kg, body weight). The third was the curcumin group (animals received a daily dose of 20mg/kg body weight of curcumin dissolved in 2ml/kg body weight of olive oil).  The fourth group was the combination group, where animals received oral doses of curcumin as in the third group, followed by a single oral dose of NaNo2 after 4 weeks of treatment. 48 hours after oral NaNO₂, animals were sacrificed, and samples were collected for serum and tissue markers of hepatic injury, oxidative stress, and lipid profile.

Results:  The use of a single oral dose of NaNo2 was associated with significant increase of hepatic injury indicators (e.g., ALT, AST, and ALP) when compared to control group. In addition, this group had dyslipidemia and a significant increase of oxidative stress indicators than the control group. The use of curcumin prior to administration of NaNO2 ameliorate these toxic effects but it did not abolish it, as there was a significant difference in combined than control and NaNO2 groups.

Conclusion: : A single oral dose of NaNO2 had a hepatotoxic effect. Curcumin had a prophylactic effect when administered prior to exposure to NaNO2. These actions are produced via modulation of antioxidant status.