In the present study, the possible protective effects of gallic acid isolated from Peltiphyllum peltatum against sodium fluoride (NaF)-induced hepatotoxicity and oxidative stress were evaluated. Rats were intoxicated with 600ppm NaF through drinking water for one week. Gallic acid (10 and 20mg/kg) and the positive control, silymarin (10mg/kg) were administrated for seven days prior to NaF intoxication. 24h after the treatment period, superoxide dismutase and catalase activities, lipid peroxidation and reduced glutathione levels were measured in the liver. Serum biochemical markers including: alanine transaminase, aspartate aminotransferase, alkaline phosphatase, lipase and α-amylase activities and triglyceride, cholesterol, glucose, total bilirubin, direct bilirubin, total protein and albumin levels were determined. The results demonstrated that pretreatment with gallic acid normalized the sodium fluoride-induced alterations in serum parameters and oxidative stress in hepatic tissue. Fluoride intoxication resulted in an increased level of thiobarbituric acid reactive substances (TBARS) (53.05±2.23nmol MDA equiv./g tissue) in the liver homogenates in comparison with control group (25.03±1.27nmol MDA equiv./g tissue). Pretreatment with gallic acid at 20mg/kg demonstrated significant mitigation in TBARS level (33.95±2.51nmol MDA equiv./g tissues). Fluoride intoxication did also suppress the superoxide dismutase and catalase activity of hepatic tissue homogenates by 33.87% and 66.87%, respectively. Treatment with gallic acid resulted in a dose-dependent mitigation of the fluoride-mediated suppression of antioxidant enzymes. In conclusion, gallic acid prevented the NaF-induced abnormalities in the serum and hepatic biochemical markers.