Paper Title
Antioxidant Actions Of Nicotinamide And Aminoguanidine Protect Against Allyl Alcohol Induced Hepatotoxicity In Mice

Abstract
Allyl alcohol (AA) is a widely used chemical that exhibits selective hepato-toxicity which is mediated through its metabolite acrolein resulting in liver necrosis. Damage to the liver by hepatotoxic chemicals has grave consequences and may be mediated through different mechanisms including oxidative stress and a decrease in cellular ATP. In this study we investigated the hepatoprotective potential of Nicotinamide a selective poly (ADP ribose) synthetase (PARS) inhibitor and Aminoguanidine a selective NO synthase (iNOS) inhibitor and a peroxynitrite scavenger on Allyl alcohol induced hepato toxicity in Swiss albino mice. Male mice weighing 25 - 30 g were used in the study. Allyl alcohol (1.5mmol/ Kg ) was administered intra-peritoneally. Separate groups (6 animals each) of mice were administered Nicotinamide and Aminoguanidine in doses of 100mg/Kg, 30 minutes before the administration of AA. Blood and liver samples were collected 4 hours after the administration of AA to study the changes in serum Alanine amino transferase, (AT), and hepatic lipid peroxides, and glutathione levels. AA administration significantly elevated the serum AT levels and the hepatic lipid peroxides and resulted in a decrease in the GSH contents of the liver. Prophylactic administration of both Nicotinamide and Aminoguanidine showed significant hepato protective effects. They significantly decreased the AA induced increase in AT and lipid peroxides and replenished the depleted GSH levels. The results of this study suggest that both Nicotinamide and Aminoguanidine significantly decrease the hepatotoxic effects of Allyl alcohol. They further suggest the involvement of NO and PARS in AA induced hepatotoxicity.