Efficacy and Safety of Folic Acid During Toxic Hepatitis Induced by Acute Overdose of Paracetamol

Paracetamol, a major cause of acute liver failure represents a significant clinical problem. Intake of a large dose of paracetamol (APAP) may result in severe hepatic necrosis. Oxidative stress mediated by oxidative capacities of the APAP metabolite (N-acetyl-P-benzoquinon-imine (NAPQI)) is considered as the main cause of hepatotoxicity of APAP. This labor therefore seeks to induce liver damage in rats using single dose of APAP and to evaluate the possible protective effects of administration of folic acid on APAP induced liver damage in rats. Serum transaminases and lactic dehydrogenase levels were assessed as markers of hepatic damage. Also, bilirubin, total protein, albumin, globulin and A/G ratio were analyzed. Equally, comparative effects of folic acid on the markers were also evaluated. Paracetamol caused liver damage as evident by statistically significant increased in the activities of alanine aminotransferase, aspartate aminotransferase and alkaline phosphates. There were general statistically significant losses in the activities of lactic dehydrogenase and an increase in total bilirubin and protein with significant decrease in A/G ratio in paracetamol treated group compared with the control group. Also, the histopathological examination of liver showed marked degeneration of hepatic cells and necrosis with congested portal vein and dilated hepatic sinusoid. However, folic acid was able to counteract the effect of APAP. The present results suggest that folic acid can act as hepatoprotective against paracetamol toxicity and that the mechanism by which they do this is by acting as antioxidants.