The relationship between free radical and scavenger enzymes has been found in the epilepsy and reactive oxygen species have been implicated in seizure-induced neurodegeneration. It has been suggested that pilocarpine-induced seizures is mediated by increases in oxidative stress. Current researches have suggested that antioxidant compounds may afford some level of neuroprotection against the neurotoxicity of seizures in cellular level. The objective of the present study was to evaluate the neuroprotective effects of lipoic acid (LA) in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with 0.9% saline (i.p., control group), LA (20mg/kg, i.p., LA group), pilocarpine (400mg/kg, i.p., P400 group), and the association of LA (20mg/kg, i.p.) plus pilocarpine (400mg/kg, i.p.), 30min before of administration of LA (LA plus P400 group). After the treatments all groups were observed for 1h. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline and pilocarpine-treated animals. Protective effects of LA were also evaluated on the same parameters. In P400 group there was a significant increase in lipid peroxidation, nitrite level and glutathione peroxidase (GPx) activity. However, no alteration was observed in superoxide dismutase (SOD) and catalase activities. Antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content as well as increased the SOD, catalase and GPx activities in rat striatum after seizures. Our findings strongly support the hypothesis that oxidative stress in striatum occurs during seizures induced by pilocarpine, proving that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and also imply that strong protective effect could be achieved using LA.