The purpose of this study was to examine the potential cardioprotective role of gallic acid, a natural phenolic
acid isolated from Peltiphyllum peltatum, against sodium fluoride-induced oxidative stress in rat’s heart. Oxidative stress
and cardiotoxicity were induced by drinking water containing 600 ppm of sodium fluoride (NaF) for a week. For determination
of cardioprotective role of gallic acid, 10 and 20 mg/kg doses were intraperitoneally administrated daily for a week
prior to NaF intoxication. Thiobarbituric acid reactive substances (TBARS), antioxidant enzyme activities (i.e. superoxide
dismutase and catalase) and the level of non-enzymatic antioxidant (reduced glutathione) were evaluated in the homogenates
of rat’s cardiac tissues. Vitamin C (10 mg/kg) was used as standard antioxidant for comparison. Thiobarbituric acid
reactive substance levels in heart homogenates of NaF intoxicated rats significantly increased (59.36 ± 2.19 nmol MDA
eq/g tissue) when compared with control group (43.51 ± 1.47 nmol MDA eq/g tissue) (P<0.001). Administration of gallic
acid at 20 mg/kg resulted in a significant decrease in TBARS levels (48.48 ± 1.81 nmol MDA eq/g tissue) (P>0.05 vs.
normal). Antioxidant enzyme activities and glutathione levels were significantly reduced in NaF-treated animals (P<0.001
vs. normal). Gallic acid of Peltiphyllum peltatum at 20 mg/kg totally reversed (P>0.05 vs. control group) the oxidative
stress induced by NaF as evidenced from the measured biochemical markers: superoxide dismutase (102.21 ± 1.29 U/g
tissue) and catalase (39.29 ± 1.49 μmol/min/mg protein) activities and reduced glutathione (5.11 ± 0.09 μg/mg protein)
levels. We concluded that gallic acid mitigated NaF induced oxidative stress in rat heart.