Freitas R M, Nascimento V S, Vasconcelos S M M, Sousa F C F, Viana G S B, Fonteles M M F
Laboratory of Neuropharmacology, Department of Physiology and Pharmacology, School of Medicine, Federal University of Ceará, Rua Frederico Severo 201, Ap 103, Bl 07, Messejana, Fortaleza 60830-310, Brazil.
Neurosci Lett. 2004 Jul 22;365(2):102-5. doi: 10.1016/j.neulet.2004.04.060.
The mechanism underlying the vulnerability of the brain to status epilepticus (SE) induced by pilocarpine remains unknown. Oxidative stress has been implicated in a variety of acute and chronic neurologic conditions, including SE. The present study was aimed at was investigating the changes in catalase activity after pilocarpine-induced seizures and SE. The Control group was treated with 0.9% saline (NaCl, subcutaneously (s.c.)) and sacrificed 1h after the treatment. Another group was treated with pilocarpine (400 mg/kg, s.c., Pilocarpine group) and sacrificed 1h after treatment. The catalase activity in the cerebellum, hippocampus, frontal cortex and striatum of Wistar rats was determined. The results have shown that pilocarpine administration and resulting SE produced a significant increase in the catalase activity in the hippocampus (36%), striatum (31%) and frontal cortex (15%) of treated adult rats. Nevertheless, in the adult rat cerebellum after SE induced by pilocarpine no change was observed in the catalase activity. Our results demonstrated a direct evidence of an increase in the activity of the scavenging enzyme (catalase) in different cerebral structures during seizure activity that could be responsible for eliminating oxygen free radicals and might be one of the compensatory mechanisms to avoid the development of oxidative stress during the establishment of SE induced by pilocarpine. Our reports also indicate clear regional differences in the catalase activity caused by pilocarpine-induced seizures and SE and the hippocampus might be the principal area affected and cerebellum does not modify for this parameter studied during epileptic activity.
毛果芸香碱诱发癫痫持续状态(SE)时大脑易损性的潜在机制尚不清楚。氧化应激与包括SE在内的多种急慢性神经系统疾病有关。本研究旨在调查毛果芸香碱诱发癫痫发作和SE后过氧化氢酶活性的变化。对照组皮下注射0.9%生理盐水(NaCl),注射后1小时处死。另一组皮下注射毛果芸香碱(400mg/kg,毛果芸香碱组),注射后1小时处死。测定Wistar大鼠小脑、海马、额叶皮质和纹状体中的过氧化氢酶活性。结果表明,给予毛果芸香碱并导致SE后,成年大鼠海马(36%)、纹状体(31%)和额叶皮质(15%)中的过氧化氢酶活性显著增加。然而,在毛果芸香碱诱发SE后的成年大鼠小脑中,未观察到过氧化氢酶活性的变化。我们的结果直接证明了癫痫发作活动期间不同脑结构中清除酶(过氧化氢酶)活性增加,这可能负责清除氧自由基,并且可能是在毛果芸香碱诱发SE的过程中避免氧化应激发展产生的代偿机制之一。我们的报告还表明,毛果芸香碱诱发的癫痫发作和SE导致的过氧化氢酶活性存在明显的区域差异,海马可能是受影响的主要区域,而在癫痫活动期间,小脑在该研究参数方面没有变化。