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Nitric oxide (NO),citrulline-NO cycle enzymes,glutamine synthetase,and oxidative status in kainic acid-mediated excitotoxicity in rat brain

机译:一氧化氮(NO),瓜氨酸-NO循环酶,谷氨酰胺合成酶和海藻酸介导的大鼠兴奋性兴奋中的氧化状态

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摘要

Neuronal excitation,involving the excitatory glutamate receptors,is recognized as an important underlying mechanism in neurodegenerative disorders. To understand their role in excitotoxicity,the nitric oxide synthase (NOS),argininosuccinate synthetase (AS),argininosuccinate lyase (AL),glutamine synthetase (GS),and arginase activities,along with the concentration of nitrateitrite,thiobarbituric acid-reactive substances (TBARS),and total antioxidant status (TAS),were estimated in the cerebral cortex,cerebellum,and brain stem of rats subjected to kainic acid-mediated excitotoxicity. The results of this study clearly demonstrated the increased production of NO by increased activity of NOS. The increased activities of AS and AL suggest the increased and effective recycling of citrulline to arginine in excitotoxicity,making NO production more effective and contributing to its toxic effects. The decreased activity of GS may favor the prolonged availability of glutamic acid,causing excitotoxicity,leading to neuronal damage. The increased formation of TBARS and decreased TAS indicate the presence of oxidative stress in excitotoxicity.
机译:涉及兴奋性谷氨酸受体的神经元兴奋被认为是神经变性疾病的重要基础机制。为了了解它们在兴奋性毒性中的作用,一氧化氮合酶(NOS),精氨酸琥珀酸酯合成酶(AS),精氨酸琥珀酸酯裂解酶(AL),谷氨酰胺合成酶(GS)和精氨酸酶活性,以及​​硝酸盐/亚硝酸盐的浓度,硫代巴比妥酸反应性估计在遭受海藻酸介导的兴奋性毒性作用的大鼠的大脑皮层,小脑和脑干中所含的总胆固醇(TBARS)和总抗氧化剂状态(TAS)。这项研究的结果清楚地表明,通过增加NOS的活性可以增加NO的产生。 AS和AL的活性增加表明瓜氨酸在兴奋性毒性中再循环和有效地再循环成精氨酸,使NO的生产更有效,并有助于其毒性作用。 GS活性的降低可能有利于谷氨酸的延长可用性,引起兴奋性毒性,从而导致神经元损伤。 TBARS形成的增加和TAS的减少表明兴奋性毒性中存在氧化应激。

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