n -甲基- d -天冬氨酸对小鼠各脏器超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶活性及还原型谷胱甘肽水平的影响。

Waldemar Szaroma, K Dziubek, E Kapusta
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引用次数: 11

摘要

n -甲基- d -天冬氨酸受体(NMDARs)是一类主要的异离子型谷氨酸受体。受体激活招募,通过钙信号转导机制在氧化代谢,线粒体自由基的产生和其他线粒体因素的发生中发挥重要作用,这些因素可能导致兴奋性毒性和神经元死亡。本研究探讨了n -甲基- d -天冬氨酸(NMDA)刺激脑、肝、肾和胰腺NMDARs对血液、脑、肝和肾中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSHPx)活性及还原性谷胱甘肽(GSH)量的影响。NMDA是一种NMDA受体的激动剂,在给药后,被检查器官中SOD、CAT和GSHPx的活性以及还原性谷胱甘肽(GSH)的量均有统计学意义上的降低,这表明NMDA给药损害了小鼠被研究器官的抗氧化状态。
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Effect of N-methyl-D-aspartic acid on activity of superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione level in selected organs of the mouse.

One of the major classes of ionotropic glutamate receptors is the class of N-methyl-D-aspartate receptors (NMDARs). Receptor activation recruits, via calcium signal transduction mechanisms which play important roles in oxidative metabolism, mitochondrial free radical production and occurrence of other mitochondrial factors which potentially contribute to excitotoxicity and neuronal death. In the present study, the effects of stimulation of NMDARs by applying N-methyl-D-aspartic acid (NMDA) in the brain, liver, kidneys and pancreas on change of the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx) and in the amount of reduced glutathione (GSH) in blood, brain, liver and kidneys has been investigated. Statistically significant decrease of the activity of SOD, CAT and GSHPx and in the amount of reduced glutathione (GSH) was found in the examined organs after administration of NMDA, an agonist of NMDA receptors, demonstrating that NMDA administration compromises the antioxidant status in the investigated organs of the mouse.

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来源期刊
Acta physiologica Hungarica
Acta physiologica Hungarica 医学-生理学
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