Regional susceptibility to oxidative stress in a model of experimental epilepsy.

LORES ARNAIZ, S.; TRAVACIO, M.; LLESUY, S.; RODRÍGUEZ DE LORES ARNAIZ, G.

New Orleans, Louisiana

Congreso; 30th Annual Meeting American Society for Neurochemistry; 1999

American Society for Neurochemistry

Oxidative stress associated with a model of experimental epilepsy was evaluated. Male Wistar rats were injected i.p. with 150 mg/kg convulsant 3-meracptopropionic acid and decapitated in two stages: during seizures or in the post-seizure period. Spontaneous chemiluminescence, levels of thiobarbituric acid reactive susbtances, total antioxidant capacity and antioxidant enzyme activities were measured in cerebellum, hippocampus, cerebral cortex and striatum. In animals killed at seizure, increases of 42% and 90% were observed in spontaneous chemiluminescence of cerebellum and cerebral cortex homogenates respectively, accompanied by a 25% increase in cerebral cortex levels of thiobarbituric reactive substances. In the post-seizure stage, emission completely recovered control levels in cerebral cortex and partially in cerebellum, thus showing oxidative stress reversibility in time. Hippocampus and striatum seemed less vulnerable to oxidative damage. A 30% decrease in glutathione peroxidase activity was only observed in cerebral cortex during seizures, while catalase and superoxide dismutase remained unchanged in all four areas during either stage. Likewise, total antioxidant capacity was unaffected in any of the studied areas. It is suggested that oxidative stress in this model of epilepsy arises from an increase in oxidant species rather than from depletion of antioxidant defences.