The present study was designed to estimate the protective effect of (-) epigallocatechin gallate(EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day × 60 days)caused liver damage that was manifested by the elevation of markers of liver dysfunction -aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase,bilirubin and γ-glutamyl transferase in plasma and reduction in liver glycogen. The activities ofalcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase werefound to be altered in alcohol-treated group. Ethanol administration resulted in the induction ofcytochrome p450 and cytochrome-b5 activities and reduction of cytochrome-c reductase andglutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced theviability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and inducedhepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats withEGCG restored the levels of markers of liver injury and mitigated the alterations in alcoholmetabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viabilityand reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findingssuggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.