脑内高铁在帕金森病病因中的作用

对帕金森病的病理研究发现黑质内存在氧化应激状态是由于铁在黑质致密带多巴胺能神经元内选择性堆积的结果。实验已证实铁负载引起卢的氧化应激导致的生化变化与帕金森病黑质内的改变是一致的，黑质内注射铁可选择性损伤多巴胺能神经元，模拟帕金森病的生化及行为改变，最近对6-羟基多巴的神经毒性与其能从铁蛋白中释放铁的有关研究，更加证实了铁诱导产生氧自由基参与黑质纹状体多巴胺能神经元变性，对铁鳌合剂去铁胺的研究也证实了这一观点。

High brain iron in etiology of Parkinson's disease

The recently described pathology of Parkinson's disease supports the view for a state of oxidative stress in the substantia nigra (SN), resulting as a consequence of the selective accumulation of iron in SN zona compacta and within the melanized dopamine neurons. The biochemical changes due to oxidative stress resulting from tissue iron overload are similar to those now being identified in parkinsonian SN. Intranigral iron injection in rats produces a selective lesioning of dopamine neurons, resulting in a behavioral and biochemical parkinsonism. The participation of iron-induced oxygen free radicals in the process of nigrostriatal dopamine neuron degeneration is strengthened by recent studies in which the neurotoxicity of 6-OHDA had been linked to the release of iron from its binding sites in ferritin. This is further supported by experiments with the iron chelator desferrioxamine.