Oxidative stress in the hippocampus after pilocarpine‐induced status epilepticus in Wistar rats

Abstract

Status epilepticus (SE) is a neurological emergency with an associated mortality of 10-12% [1]. Pilocarpine-induced seizure models have provided information on the behavioral and neurochemical characteristics associated with seizure activity [2,3]. Other studies suggest permanent changes in different biochemical systems during SE. An increase in lipid peroxidation, a decrease in GSH content, and excessive free radical formation may occur during SE induced by pilocarpine [4,5].This model can be used to investigate the development of neuropathology in SE [6]. Despite numerous studies clearly indicating the importance of enzyme activity in the epileptic phenomenon, the mechanisms by which these enzymes influence SE are not completely understood [7,8]. Therefore, we decided to study enzymatic activity related to oxidative stress mechanisms during SE [9].Oxidative stress, which is defined as the over-production of free radicals, can dramatically alter neuronal function and has been related to SE [10,11]. It is particularly facilitated in the brain, as the brain contains large quantities of oxidizable lipids and metals, and, moreover, has fewer antioxidant mechanisms than other tissues [8].Free radicals are chemical entities characterized by an orbital containing an unpaired electron [12]. This electron confers on these molecules a strong propensity to react with target molecules by giving or withdrawing one electron from the target molecules to complete their own orbital [13]. Superoxide, a free radical, can be generated in the brain by several mechanisms such as The role of oxidative stress in pilocarpine-induced status epilepticus was investigated by measuring lipid peroxidation level, nitrite content, GSH concentration, and superoxide dismutase and catalase activities in the hippocampus of Wistar rats. The control group was subcutaneously injected with 0.9% saline. The experimental group received pilocarpine (400 mgAEkg )1 , subcutaneous). Both groups were killed 24 h after treatment. After the induction of status epilepticus, there were significant increases (77% and 51%, respectively) in lipid peroxidation and nitrite concentration, but a 55% decrease in GSH content. Catalase activity was augmented 88%, but superoxide dismutase activity remained unaltered. These results show evidence of neuronal damage in the hippocampus due to a decrease in GSH concentration and an increase in lipid peroxidation and nitrite content. GSH and catalase activity are involved in mechanisms responsible for eliminating oxygen free radicals during the establishment of status epilepticus in the hippocampus. In contrast, no correlations between superoxide dismutase and catalase activities were observed. Our results suggest that GSH and catalase activity play an antioxidant role in the hippocampus during status epilepticus.Abbreviations ROS, reactive oxygen species; SE, status elipticus.

Assessment of effect of ethanolic extract of Tephrosia purpurea (L.) Pers., Fabaceae, activity on lithium-pilocarpine induced Status epilepticus and oxidative stress in Wistar rats

“…There is clinical and experimental evidence of reduced oxygen availability after status epilepticus. Evidence for the role of free radicals in status epilepticus has been found by using enzymatic and nonenzymatic antioxidant treatment for the protection against seizures and for status epilepticus -induced neuronal damage (Freitas et al, 2005).…”

Superoxide dismutase and catalase activities in rat hippocampus pretreated with garcinielliptone FC fromPlatonia insignis

“…Our findings showed that GFC, DMF, EAF, EE, or HE did not produce alterations in the hippocampus CAT activity, since they did not protect to the hippocampus from neuronal damage induced by lipid peroxidation products. It is unlikely that the unaltered CAT activity is related to the mechanisms involved in maintenance of oxidative stress (Freitas et al, 2005). These data suggest that hippocampus of rats pretreated with GFC, fractions, and extracts from P. insignis do not use CAT as the major free radical scavenging system.…”

Vigabatrina aumenta atividade da superóxido dismutase no corpo estriado de ratos após crises convulsivas induzidas pela pilocarpina

“…As crises convulsivas induzidas pela pilocarpina também estão associadas a várias mudanças neuroquímicas no corpo estriado de ratos 2 . Essas crises convulsivas podem alterar a síntese, a liberação e/ou a biotransformação de vários neurotransmissores, entre eles do GABA e glutamato 3 , como também produzem mudanças na atividade de enzimas antioxidantes 4 .…”

“…Várias alterações na concentração da peroxidação lipídica, no conteúdo do nitrito, no nível da glutationa reduzida e na atividade antioxidante enzimática foram verificadas durante a fase aguda das crises convulsivas 4 . De modo geral, os radicais livres têm sido implicados na patogênese de várias doenças neurológicas, incluindo a epilepsia.…”