Temporary clamping of the portal triad is a common strategy to minimize bleeding during livertransplantation. Increasing evidences suggests that oxygen derived free radicals and reintroduction ofoxygen in ischemic tissue lead to ischemic and reperfusion injury (I/R) and lead to apoptosis andnecrosis. Adult Wistar rat subjected to 60 min of partial liver ischemia followed by three hourreperfusion. Eighteen Wister rats were divided into sham-operated control group (I) (n = 6),ischemia and reperfusion group (II) (n = 6), folic acid treated group (1 mg/kg body weight/dailyby oral route for 7 days before induced ischemia reperfusion maneuver) (III) (n = 6). Apoptoticand necrotic hepatocytes, mitochondrial antioxidant enzymes were measured. Liver injury wasassessed by alanine transaminases (ALT), aspartate transaminases (AST), liver histopathologyand electron microscopy. An ischemic and reperfusion hepatocellular injury was indicated byincreased serum-ALT, AST, histopathology and electron microscopy studies. Apoptotic andnecrotic cells were increased which was revealed by flow cytometry in I/R group. Pre- treatmentwith folic acid significantly decreased serum -ALT, AST levels, apoptotic and necrotic cells after 1h ischemia followed by 3 h of reperfusion. Histopathology and TEM studies showed markedlydiminished hepatocellular injury in folic acid pretreated rats during the hepatic I/R, whichreached a level comparable to saline-treated rat of sham operated group. On the basis of ourfindings it may be concluded that folic acid afforded significant protection from necrosis andapoptosis in I/R injury.