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.
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The work was supported by grant 1.64 SSRP of the Republic of Belarus “Biotechnologies,” 2016–2020.
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Ethical approval. All the experiments with animals were conducted in compliance with ethical standards and rules on the use of experimental animals in scientific research composed on the basis of Directive 2010/63/EU of the European Parliament and of the Council of September 22, 2010.
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Semenovich, D.S., Lukienko, E.P. & Kanunnikova, N.P. Modulating Oxidative Stress Indices and Thiol-Disulfide Balance in the Brain Structures by Pantothenic Acid Derivatives in an Experimental Model of Parkinson’s Disease. Neurochem. J. 15, 24–29 (2021). https://doi.org/10.1134/S1819712421010128
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DOI: https://doi.org/10.1134/S1819712421010128