Protective role of gallic acid on sodium fluoride induced oxidative stress in rat brain.

Gallic acid is known as a potent antioxidant active compound of the edible and medicinal plant Peltiphyllum peltatum. The main objective of this study was to evaluate the neuroprotective effects of gallic acid against sodium fluoride induced oxidative stress in rat brain. Gallic acid (10 and 20 mg/kg) and vitamin C (10 mg/kg) were intraperitoneally administrated for 1 week prior to sodium fluoride intoxication. After the treatment period, brain tissues were collected and homogenized, and antioxidant parameters were measured in the homogenates. The level of thiobarbituric acid reactive substances in sodium fluoride intoxicated rats (42.04 ± 2.14 nmol MDA eq/g tissue, p < 0.01 vs. normal) increased compared to the normal rats (35.99 ± 1.08 nmol MDA eq/g tissue). Pretreatment with gallic acid at 20 mg/kg was exhibited significant reduction in the thiobarbituric acid reactive substances level (37.06 ± 1.4 nmol MDA eq/g tissue, p > 0.05 vs. normal). This increasing in thiobarbituric acid reactive substances level was accompanied with a decrease in the level of reduced glutathione (6.74 ± 0.28 μg/mg of protein, p < 0.001 vs. normal), superoxide dismutase (53.24 ± 1.62 U/mg of protein, p < 0.001 vs. normal) and catalase (70.73 ± 2.94 μmol/min/mg of protein p < 0.001 vs. normal) activities in sodium fluoride intoxicated rat. Gallic acid at 20 mg/kg was significantly modified the level of reduced glutathione (11.02 ± 0.53 μg/mg of protein, p < 0.05 vs normal) and catalase activity (89.22 ± 3.67 μmol/min/mg of protein, p > 0.05 vs. normal) in rat brain. However, gallic acid at 20 mg/kg was significantly more effective in retrieving superoxide dismutase (124.78 ± 5.7 U/mg of protein) activity than vitamin C (115.5 ± 4.97 U/mg of protein).