Ahlskog J E, Uitti R J, Low P A, Tyce G M, Nickander K K, Petersen R C, Kokmen E
Department of Neurology, Mayo Clinic Rochester, Minnesota 55905, USA.
Mov Disord. 1995 Sep;10(5):566-73. doi: 10.1002/mds.870100507.
Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemical abnormalities extending beyond the central nervous system have been identified in patients with this condition. Previous investigators have found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Parkinson's disease. We attempted to replicate these findings but controlled for other factors that could influence malondialdehyde levels. We detected no significant elevations in mean serum malondialdehyde concentrations in either levodopa-treated or untreated patients with Parkinson's disease, compared to normal controls; similarly, no elevation was found in a group of patients with dementia of Alzheimer's type. On the other hand, a group of subjects with diabetes mellitus but no neurodegenerative disease had significantly elevated mean serum malondialdehyde levels, consistent with previous studies of diabetic patients. Autoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxidation product of dopa, 5-S-cysteinyl-dopa, in the plasma of these same groups of patients with neurodegenerative disease and normal controls; no significant differences were identified. Serum concentrations of two other antioxidant substances, alpha-tocopherol and uric acid, were also statistically similar in these groups. In conclusion, analysis of several blood products relevant to oxidant stress, including malondialdehyde, 5-S-cysteinyl-dopa, alpha-tocopherol, and uric acid, failed to distinguish patients with Parkinson's disease or dementia of Alzheimer's type from controls.
多巴胺代谢继发的氧化应激被认为是帕金森病发病机制中的一个致病因素。患有这种疾病的患者已被发现存在超出中枢神经系统的生化异常。先前的研究人员发现帕金森病患者血浆和血清中脂质过氧化产物丙二醛的浓度异常升高。我们试图重复这些发现，但对可能影响丙二醛水平的其他因素进行了控制。与正常对照组相比，我们发现左旋多巴治疗的或未治疗的帕金森病患者血清丙二醛平均浓度均无显著升高；同样，在一组阿尔茨海默型痴呆患者中也未发现升高。另一方面，一组患有糖尿病但无神经退行性疾病的受试者血清丙二醛平均水平显著升高，这与先前对糖尿病患者的研究一致。自氧化是多巴胺和多巴代谢产生氧自由基的两条主要途径之一。我们分析了这些患有神经退行性疾病的患者组和正常对照组血浆中多巴的自氧化产物5-S-半胱氨酰多巴；未发现显著差异。这些组中另外两种抗氧化物质α-生育酚和尿酸的血清浓度在统计学上也相似。总之，对与氧化应激相关的几种血液成分（包括丙二醛、5-S-半胱氨酰多巴、α-生育酚和尿酸）的分析未能区分帕金森病患者或阿尔茨海默型痴呆患者与对照组。
