Kang Jung Hoon
Department of Genetic Engineering, Chongju University, Chongju 360-764, Korea.
J Biochem Mol Biol. 2004 May 31;37(3):325-9. doi: 10.5483/bmbrep.2004.37.3.325.
Oxidation of catecholamines may contribute to the pathogenesis of Parkinson's disease (PD). The effect of the oxidized products of catecholamines on the modification of Cu,Zn-superoxide dismutase (SOD) was investigated. When Cu,Zn-SOD was incubated with the oxidized 3,4-dihydroxyphenylalanine (DOPA) or dopamine, the protein was induced to be aggregated. The deoxyribose assay showed that hydroxyl radicals were generated during the oxidation of catecholamines in the presence of copper ion. Radical scavengers, azide, N-acetylcysteine, and catalase inhibited the oxidized catecholamine-mediated Cu,Zn-SOD aggregation. Therefore, the results indicate that free radicals may play a role in the aggregation of Cu,Zn-SOD. When Cu,Zn-SOD that had been exposed to catecholamines was subsequently analyzed by an amino acid analysis, the glycine and histidine residues were particularly sensitive. These results suggest that the modification of Cu,Zn-SOD by oxidized catecholamines might induce the perturbation of cellular antioxidant systems and led to a deleterious cell condition.
儿茶酚胺的氧化可能与帕金森病（PD）的发病机制有关。研究了儿茶酚胺氧化产物对铜锌超氧化物歧化酶（SOD）修饰的影响。当铜锌SOD与氧化的3,4-二羟基苯丙氨酸（DOPA）或多巴胺一起孵育时，该蛋白质会被诱导聚集。脱氧核糖分析表明，在铜离子存在下儿茶酚胺氧化过程中会产生羟基自由基。自由基清除剂叠氮化物、N-乙酰半胱氨酸和过氧化氢酶可抑制氧化儿茶酚胺介导的铜锌SOD聚集。因此，结果表明自由基可能在铜锌SOD的聚集中起作用。当对暴露于儿茶酚胺的铜锌SOD进行氨基酸分析时，发现甘氨酸和组氨酸残基特别敏感。这些结果表明，氧化儿茶酚胺对铜锌SOD的修饰可能会引起细胞抗氧化系统的紊乱，并导致有害的细胞状态。
