WHY ARE NIGRAL CATECHOLAMINERGIC NEURONS MORE VULNERABLE THAN OTHER CELLS IN PARKINSONS-DISEASE
WHY ARE NIGRAL CATECHOLAMINERGIC NEURONS MORE VULNERABLE THAN OTHER CELLS IN PARKINSONS-DISEASE
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DOI：
10.1002/ana.410320715
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发表时间：
1992-01-01
影响因子：
11.2
通讯作者：
HIRSCH, EC
中科院分区：
文献类型：
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作者：
HIRSCH, EC
虽然帕金森氏病神经元死亡的原因尚不清楚，但过氧化现象已被认为是一种潜在的细胞毒性机制。含有神经黑色素（一种儿茶酚胺的自氧化副产物）的儿茶酚胺能神经元在帕金森病中比非黑色素化的儿茶酚胺能神经元更脆弱。高水平的铜锌超氧化物歧化酶mRNA已被观察到在黑质，这表明高水平的氧自由基确实产生的结构。在帕金森病中，被低密度谷胱甘肽过氧化物酶细胞包围的儿茶酚胺能神经元比那些受到良好保护的氧化应激细胞更容易变性。铁中的黑质含量在帕金森病中增加，铁是一种加剧儿茶酚胺能神经元中自由基产生的化合物。总之，这些数据表明，过氧化可能参与选择性的脆弱性，在帕金森氏病的儿茶酚胺能神经元。
Although the cause of neuronal death in Parkinson's disease remains unknown, a hyperoxidation phenomenon has been implicated as a potential cytotoxic mechanism. Catecholaminergic neurons containing neuromelanin, an autoxidation byproduct of catecholamines, are more vulnerable in Parkinson's disease than nonmelanized catecholaminergic neurons. High levels of CuZn superoxide dismutase mRNA have been observed in the substantia nigra, suggesting that high levels of oxygen free radicals are indeed produced in the structure. Catecholaminergic neurons surrounded by a low density of glutathione peroxidase cells are more susceptible to degeneration in Parkinson's disease than those well protected against oxidative stress. The nigral content in iron, a compound that exacerbates the production of free radicals in catecholaminergic neurons, is increased in Parkinson's disease. Altogether these data suggest that hyperoxidation may participate in the selective vulnerability of catecholaminergic neurons in Parkinson's disease.