Introduction: Oxidative stress is one of the prime pathogenic factors going on in both human epilepsy and experimental epileptogenic models. PTZ-Seizure has been associated with over production of superoxide anion, reduced GSH levels, increased lipid peroxidation and protein oxidation in the hippocampus. Methodology: Forty male wistar rats were divided into 5 groups (normal saline, 200 mg/kg sodium valporate, 25% PMS, 50 % PMS and 100 % PMS) with each group receiving PTZ (35 mg/kg) on every alternate day for 30 days. Thirty minutes after each PTZ injection rats were observed for seizure behavior using the Racine scale. The hippocampal tissues were isolated, homogenized and used to determine SOD, CAT, GSH and MDA level. Result: This result revealed significant increase in the mean hippocampal SOD activity of PTZ-kindled wistar rats fed with PMS [25% (18.90 ± 1.08), 50% (18.90 ± 1.08, 24.90 ± 1.37) and 100 % (11.06 ± 0.58 IU/ mg protein) when compared to normal saline group (8.84 ± 0.96 IU/ mg protein). PM Supplementation increased mean CAT activity at 25% and 50% [25% (12.68 ± 0.68), 50% (8.74 ± 0.92) and 100% (15.66 ± 1.12 µg/ mg protein)] Vs normal saline treated group (9.60 ± 0.72 µg/ mg protein). A significant increase in mean hippocampal GSH concentration was seen in all the PMS fed wistar rats [25 % (29.52 ± 0.44), 50 % (24.42 ± 1.51) and 100 % (40.32 ± 1.43 µg/ mg protein)] when compared to normal saline (10.88 ± 0.32 µg/ mg protein). PTZ-kindled wistar rats fed with PMS [25% (86.62 ± 2.81), 50% (73.86 ± 3.26) and 100% (73.56 ± 1.82 nmol/ mg protein) showed significant decrease in the mean concentration of hippocampal MDA when compared to normal saline (119.90 ± 2.34 nmol/ mg protein). Conclusion: Supplementation with PG inhibits hippocampal redox imbalance and reinforces it antioxidant system.