Abstract
Previous experiments have shown that the generation of free radicals in rat brain homogenates is increased following pilocarpine-induced seizures and status epilepticus (SE). This study was aimed at investigating the changes in neurochemical mechanisms such as lipid peroxidation levels, nitrite content, glutathione reduced (GSH) concentration, superoxide dismutase and catalase activities in the frontal cortex and the striatum of Wistar adult rats after seizures and SE induced by pilocarpine. The control group was treated with 0.9% saline and another group of rats received pilocarpine (400 mg/kg, i.p.). Both groups were sacrificed 24 h after the treatments. Lipid peroxidation level, nitrite content, GSH concentration and enzymatic activities were measured by using spectrophotometric methods. Our findings showed that pilocarpine administration and its resulting seizures and SE produced a significant increase of lipid peroxidation level in the striatum (47%) and frontal cortex (59%). Nitrite contents increased 49% and 73% in striatum and frontal cortex in pilocarpine group, respectively. In GSH concentrations were decreases of 54% and 58% in the striatum and frontal cortex in pilocarpine group, respectively. The catalase activity increased 39% and 49% in the striatum and frontal cortex, respectively. The superoxide dismutase activity was not altered in the striatum, but it was present at a 24% increase in frontal cortex. These results suggest that there is a direct relationship between the lipid peroxidation and nitrite contents during epileptic activity that can be responsible for the superoxide dismutase and catalase enzymatic activity changes observed during the establishment of seizures and SE induced by pilocarpine.
Highlights
A literature review revealed that there are articles that address the role of oxidative stress in neurological disorders, including seizure models induced by pilocarpine in which the modulation of the pro-oxidant/ antioxidant balance by seizures per se and by antioxidant agents is discussed.[1,2,25]
Lipid peroxidation in a tissue is an index of irreversible biological damage of the cell membrane phospholipid, which in turn leads to inhibition of most of the sulphydryl and some nonsulphydryl enzymes.[26,27]
Lipid peroxidation can be induced by many chemicals and by many tissue injuries, and it has been suggested as a possible mechanism for the neurotoxic effects observed during epileptic activity.[7,26]
Summary
Numerous neurochemical studies using animals have revealed that oxidative stress-related seizures produce changes in antioxidant enzymatic activity and receptor binding.[1,2,3] Oxidative stress-related brain disorders, including epilepsy, showed a substantial decrease in cholinergic markers, such as acetylcholinesterase[4] and a number of muscarinic receptors in the hippocampus, striatum and frontal cortex of adult rats.[5,6] Epilepsy is a complex neurobehavioral disorder that can be the result of increased excitability of neurons in several brain regions.[7,8] Pilocarpine administration makes it progresse to a long-lasting SE within 1–2 h and induces behavioral and electroencephalographic alterations which are similar the TLE in humans.[9] Epilepsy model induced by pilocarpine in rodents can provide information regarding oxidative stress-related epileptic activity.[10,11,12] TLE can be characterized by a permanent change in OS that is more facilitated in the brain in relation to others tissues because it contains large quantities of oxidizable lipids and metals and a lower number of antioxidant defenses.[13,14]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
