Abstract—We studied changes in the indices of free-radical oxidation and thiol-disulfide status in the brain structures in the experimental model of Parkinson’s disease (PD) induced by administration of rotenone to rats. Pantothenic acid derivatives, such as panthenol (PL), pantethine (PT), and homopantothenic acid (HPA) were used as neuromodulators. It was found that redox imbalance in the brain induced by rotenone is accompanied by the activation of free-radical processes, pronounced inhibition of antioxidant defense, a considerable decrease in the glutathione system reduction potential, and increased protein glutathionylation. The strongest changes were in the basal ganglia of the brain. PL and PT but not HPA, decrease the changes in the free-radical oxidation and thiol-disulfide balance in the brain structures. During experimental neurotoxicosis, the mechanisms of neuroprotective action of PL and PT, which are linked with the changes in the biosynthesis of CoA, are, obviously, related to their ability to increase the reduction potential of the glutathione system, thus mitigating the effects of oxidative stress.

摘要-我们研究了鱼藤酮对大鼠诱发的帕金森病（PD）实验模型中脑结构中自由基氧化指数和巯基-二硫键状态的变化。泛酸衍生物，如泛醇（PL），泛硫氨酸（PT）和高泛酸（HPA）被用作神经调节剂。发现鱼藤酮诱导的大脑中的氧化还原失衡伴随着自由基过程的激活，抗氧化防御的明显抑制，谷胱甘肽系统还原潜力的显着降低以及蛋白质谷胱甘肽酰化的增加。最强烈的变化是在大脑的基底神经节。PL和PT而不是HPA降低了大脑结构中自由基氧化和巯基-二硫键平衡的变化。在实验性神经毒症中