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首页> 外文期刊>Journal of neurology >Is levodopa toxic?
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Is levodopa toxic?

机译：左旋多巴有毒吗？

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The objective of this workshop was to review and discuss the debate on neurotoxicity of levodopa in the treatment of Parkinson's disease (PD) with consideration of preclinical and clinical findings. We concluded that in particular preclinical outcomes of in vitro models of neurodegeneration describe neurotoxic effects of levodopa, whereas trials in animal models provided controversial results. To date, clinical trials in PD patients showed no convincing proof of direct neurotoxic effects of levodopa on progression of neurodegeneration with various applied functional imaging techniques particularly with specific radiotracers for nigral dopaminergic neurotransmission. However, the controversy on neurotoxicity of levodopa only partially considered indirect mechanisms, i. e. levodopa-associated homocysteine elevation. But there is accumulating evidence that this long-term side effect of chronic levodopa administration dose dependently individually contributes to progression of neurodegeneration due to increased release of neurotoxins, induction of oxidative stress and mitochondrial dysfunction according to results of in vitro and animal trials and to at least peripheral neuronal degeneration and increased risk for onset of atherosclerosis-related disorders according to clinical trials in PD patients. From this point of view we demand that future research on the efficacy and putative neurotoxicity of antiparkinsonian compounds should also consider putative toxic long-term effects of drug administration and should look for putative peripheral biomarkers and individual, environmental or nutritative risk factors in order to establish a preventive therapy, i. e. folic acid administration in the case of levodopa-associated homocysteine elevation.
机译：这次研讨会的目的是回顾和讨论有关左旋多巴治疗帕金森氏病（PD）的神经毒性的辩论，同时考虑临床前和临床发现。我们得出的结论是，特别是神经变性体外模型的临床前结果描述了左旋多巴的神经毒性作用，而在动物模型中的试验提供了有争议的结果。迄今为止，在PD患者中进行的临床试验没有令人信服的证据表明，左旋多巴对神经退行性疾病具有直接的神经毒性作用，这是通过各种应用的功能成像技术，特别是针对多巴胺能神经传递的特定放射性示踪剂进行的。然而，关于左旋多巴神经毒性的争论仅部分被认为是间接机制，即。 e。左旋多巴相关的同型半胱氨酸升高。但是有越来越多的证据表明，根据体外和动物试验的结果，长期服用左旋多巴的这种长期副作用会因神经毒素的释放增加，氧化应激的诱导和线粒体功能障碍而单独引起神经退行性疾病的进展。根据PD患者的临床试验，至少可以减少周围神经元变性并增加患动脉粥样硬化相关疾病的风险。从这一观点出发，我们要求对抗帕金森病化合物的功效和推定神经毒性的未来研究还应考虑药物管理的推定长期毒性作用，并应寻找推定的外周生物标志物和个体，环境或营养风险因素，以便确定预防性治疗e。左旋多巴相关的同型半胱氨酸升高的情况下叶酸的施用。

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