Meldrum B
Department of Neurology, Institute of Psychiatry, London UK.
Brain Res Brain Res Rev. 1993 Sep-Dec;18(3):293-314. doi: 10.1016/0165-0173(93)90014-q.
The possibility that some acidic amino acids occurring naturally or as additives in the diet can act as excitotoxins producing central nervous system pathology has been the subject of extensive debate in the last 20 years and is here reviewed. High doses of glutamate, aspartate or related excitatory amino acids given in isolation to neonatal rodents produce acute degeneration organs. Neuropathology resulting from consumption of glutamate or aspartate has not been described in man. Various unusual amino acids of plant origin can produce acute excitotoxic syndromes. In man domoate (consumed in mussels that have fed on (Nitschia pungens) can produce an acute syndrome associated with limbic system lesions and anterograde amnesia. Kainate and domoate produce similar syndromes in rodents; acromelate produces spinal pathology. The mechanisms and manifestations of chronic excitotoxicity are less clearly established. A combination of impaired energy metabolism or impaired buffering of calcium and free radicals and endogenous or exogenous excitotoxins may contribute to neuronal loss in human neurodegenerative disorders.
某些天然存在或作为饮食添加剂的酸性氨基酸可能作为兴奋性毒素导致中枢神经系统病变，这一可能性在过去20年里一直是广泛争论的主题，本文对此进行综述。给新生啮齿动物单独注射高剂量的谷氨酸、天冬氨酸或相关兴奋性氨基酸会导致急性器官退化。人类食用谷氨酸或天冬氨酸导致神经病理学改变的情况尚未见报道。多种植物来源的特殊氨基酸可导致急性兴奋性毒性综合征。在人类中，软骨藻酸（食用以多纹拟菱形藻为食的贻贝后摄入）可导致与边缘系统病变和顺行性遗忘相关的急性综合征。海人藻酸和软骨藻酸在啮齿动物中产生类似综合征；刺尾鱼毒素可导致脊髓病变。慢性兴奋性毒性的机制和表现尚不太明确。能量代谢受损、钙和自由基缓冲功能受损以及内源性或外源性兴奋性毒素共同作用，可能导致人类神经退行性疾病中的神经元丢失。
