Rogério Nunes dos Santos, Maria Goretti de Vasconcelos Silva and Rivelilson Mendes de Freitas
Reactive oxygen species have been implicated in seizure-induced neurodegeneration, and there is a correlation between free radical level and scavenger enzymatic activity in the epilepsy. It has been suggested that pilocarpineinduced seizures is mediated by an increase in oxidative stress. Current research has found that antioxidant may provide, in a certain degree, neuroprotection against the neurotoxicity of seizures at the cellular level. Crysophanol has numerous nonenzymatic actions and is a powerful liposoluble antioxidant. The objective of present study was to evaluate the neuroprotective effects of crysophanol (CRY) in mice, against oxidative stress caused by pilocarpineinduced seizures, 30 min prior to behavioral observation, Swiss mice were treated with, 0.9% saline (i.p., control group), CRY (0.5 mg/kg, i.p., CRY 0.5 group), CRY (1.0 mg/kg, i.p., CRY 1.0 group), pilocarpine (400 mg/kg, i.p., P400 group), or the combination of CRY (0.5 or 1.0 mg/kg, i.p.) and pilocarpine (400 mg/kg, i.p.). After the treatments all groups were observed for 24 h. The enzymatic activities and lipid per oxidation concentrations were measured using spectrophotometric methods and these data were assayed. In P400 group mice there was a significant increase in lipid peroxidation levels and catalase activity. In the CRY and pilocarpine co-administered mice, antioxidant treatment significantly reduced the lipid peroxidation level, as well as increased the catalase activities in mice hippocampus after seizures. Our findings strongly support the hypothesis that oxidative stress occurs in hippocampus during pilocarpineinduced seizures, indicate that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and imply that strong protective effect could be achieved using crysophanol.