DOES OXIDATIVE STRESS PARTICIPATE IN NERVE-CELL DEATH IN PARKINSONS-DISEASE
DOES OXIDATIVE STRESS PARTICIPATE IN NERVE-CELL DEATH IN PARKINSONS-DISEASE
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DOI：
10.1159/000118538
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发表时间：
1993-01-01
影响因子：
2.4
通讯作者：
HIRSCH, EC
中科院分区：
文献类型：
--
作者：
HIRSCH, EC
帕金森病的特征是中脑的几个细胞群中大量的神经元损失。然而，在多巴胺能系统（包括黑质神经元）中观察到最一致的病变。虽然这种神经元损失的原因仍然未知，氧化应激已被怀疑参与神经细胞死亡的机制有几个原因。(1)脂质过氧化反应是氧自由基产生的结果，已发现帕金森病患者的黑质中脂质过氧化反应升高。(2)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化的儿茶酚胺能神经元更脆弱。(3)被低密度的含有谷胱甘肽过氧化物酶（一种自由基清除酶）的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在帕金森病中变性。(4)铁的含量，一种化合物，加剧生产的自由基在儿茶酚胺能神经元，是增加在黑质帕金森氏病。然而，氧化应激是否参与疾病的原因或仅代表神经细胞死亡的结果仍有待确定。
Parkinson's disease is characterized by a massive neuronal loss in several cell groups of the midbrain. However, the most consistent lesions are observed in dopaminergic systems including nigral neurons. Although the cause of this neuronal loss remains unknown, oxidative stress has been suspected to participate in the mechanism of nerve cell death for several reasons. (1) Lipid peroxidation, a consequence of oxygen free radical production, has been found to be elevated in the substantia nigra in Parkinson's disease. (2) Catecholaminergic neurons containing neuromelanin, an autooxidation by-product of catecholamines, are more vulnerable in Parkinson's disease than non-melanized catecholaminergic neurons. (3) Catecholaminergic neurons surrounded by a low density of cells containing glutathione peroxidase, a free radical scavenging enzyme, are more susceptible to degeneration in Parkinson's disease than those well protected against oxidative stress. (4) The content of iron, a compound which exacerbates the production of free radicals in catecholaminergic neurons, is increased in the substantia nigra in Parkinson's disease. It remains, however, to be determined whether oxidative stress participates to the cause of the disease or only represents a consequence of nerve cell death.