Abstract. Physical exercise increases free radicals production; antioxidant supplementation may improve the muscle fiber’s ability to scavenge ROS and protect muscles against exercise-induced oxidative damage. This study was designed to examine the effects of all-trans resveratrol supplementation as an antioxidant to mediate anti-oxidation and lipid per-oxidation responses to exercise in male Wistar rats. Sixty-four male Wistar rats were randomly divided into four equal number (n = 16) including training + supplement (TS), training (T), supplement (S) and control (C) group. The rats in TS and S groups received a dose of 10 mg/kg resveratrol per day via gavage. The training groups ran on a rodent treadmill 5 times per week at the speed of 10 m/min for 10 min; the speed gradually increased to 30 m/min for 60 minutes at the end of 12th week. The acute phase of exercise protocol included a speed of 25 m/min set to an inclination of 10° to the exhaustion point. Superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) activity, non-enzymatic antioxidants bilirubin, uric acid, lipid peroxidation levels (MDA) and the total antioxidant capacity (TAC) were measured after the exercise termination. The data were analyzed by using one-way ANOVA. The result showed that endurance training caused a significant increase in MDA level [4.5 ± 0.75 (C group) vs. 5.9 ± 0.41 nmol/l (T group)] whereas it decreased the total antioxidant capacity [8.5 ± 1.35 (C group) vs. 7.1 ± 0.55 mmol/l (T group)] (p = 0.001). In addition, GPx and CAT decreased but not significantly (p > 0.05). The training and t-resveratrol supplementation had no significant effect on the acute response of all variables except MDA [4.3 ± 1.4 (C group) vs. 4.0 ± 0.90 nmol/l (TS group)] (p = 0.001) and TAC [8.5 ± 0.90 (C group) vs. 6.6 ± 0.80 mmol/l (TS group)] (p = 0.004). It was concluded that resveratrol supplementation may prevent exercise-induced oxidative stress by preventing lipid peroxidation.
Unique protonation states of aspartate and topaquinone in the active site of copper amine oxidase
