URIC ACID PROTECTION FROM MPTP NEUROTOXICITY

描述：选择性多巴胺神经元丢失的原因与 帕金森病（PD）未知。 人们越来越关注 了解内源性抗氧化剂在控制氧化应激中的作用 压力，以及作为潜在的治疗剂，在减缓 PD的进展。 本申请的长期目标是 尿酸作为一种内源性代谢物， 抗氧化剂 该提案描述了旨在确定是否 尿酸作为一种神经保护剂的功能， 或降低内源性尿酸水平对破坏 多巴胺细胞。 这将通过以下方法实现： 嘌呤酶抑制剂伴随多巴胺神经毒素MPTP。 这项建议的具体目的是确定尿酸的变化是否 黑质纹状体系统中的水平可以影响多巴胺细胞的程度， MPTP治疗后豚鼠死亡。

DESCRIPTION: The cause of selective dopamine neuron loss associated with Parkinson's disease (PD) is unknown. There has been growing interest in understanding the role of endogenous antioxidants in controlling oxidative stress, as well as being potential therapeutic agents in slowing the progression of PD. The long-term objective of this application is to generate experimental evidence on the role of uric acid as an endogenous antioxidant. This proposal describes experiments designed to determine if uric acid functions as a neuroprotector by investigating whether increasing or decreasing endogenous uric acid levels has an effect on the destruction of dopamine cells. This will be achieved by treating guinea pigs with purine enzyme inhibitors concomitantly with the dopamine neurotoxin MPTP. The specific aim of this proposal is to determine if changes in uric acid levels in the nigrostriatal system can influence the degree of dopamine cell death in the guinea pigs following MPTP treatment.