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 600 ppm NaF through drinking water for one week. Gallic acid (10 and the positive control, silymarin (10 mg/kg) were administrated for seven days prior to NaF intoxication. 24 h 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 -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 ± 2.23 nmol MDA equiv./g tissue) in the liver homogenates in comparison with control group (25.03 ± 1.27 nmol MDA equiv./g tissue). Pretreatment with gallic acid at 20 mg/kg demonstrated significant 20 mitigation level (33.95 ± 2.51 nmol 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%, mg/kg) in 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 biochemicalmarkers. and TBARS
