Jenner P
Parkinson's Disease Society Experimental Research Laboratories, King's College London, United Kingdom.
Neurol Clin. 1992 May;10(2):387-403.
The action of toxins or the altered metabolism of dopamine may lead to oxidative stress in substantia nigra, thereby inducing dopamine cell death and the onset of Parkinson's disease. Postmortem studies showing a depletion of reduced glutathione and increased mitochondrial superoxide dismutase activity suggest the occurrence of an ongoing toxic process in substantia nigra involving free radical mechanisms. Indeed there is a selective impairment of complex I of the mitochondrial respiratory chain in substantia nigra in Parkinson's disease, mimicking the mode of action of the selective nigral toxin MPTP. The increased formation of free radical species in substantia nigra in patients with Parkinson's disease may be accelerated by an accumulation of iron within this brain region. Altered iron metabolism and impaired mitochondrial function are not apparent in the early stages of the illness and therefore may act as accelerators of some other primary pathologic process.
毒素的作用或多巴胺代谢的改变可能导致黑质中的氧化应激,从而诱发多巴胺能细胞死亡和帕金森病的发作。尸检研究显示还原型谷胱甘肽耗竭和线粒体超氧化物歧化酶活性增加,提示黑质中存在涉及自由基机制的持续毒性过程。事实上,帕金森病患者黑质中线粒体呼吸链复合体I存在选择性损伤,类似于选择性黑质毒素MPTP的作用方式。帕金森病患者黑质中自由基的生成增加可能因该脑区铁的蓄积而加速。铁代谢改变和线粒体功能受损在疾病早期并不明显,因此可能是其他一些原发性病理过程的加速器。