vestimИзвестия Национальной академии наук Беларуси. Серия медицинских наукProceedings of the National Academy of Sciences of Belarus, Medical series1814-60232524-2350The Republican Unitary Enterprise Publishing House "Belaruskaya Navuka"10.29235/1814-6023-2018-15-1-108-118vestim-420Research ArticleОБЗОРЫREVIEWSИЗМЕНЕНИЯ ТИОЛ-ДИСУЛЬФИДНОГО БАЛАНСА ПРИ БОЛЕЗНИ ПАРКИНСОНАCHANGES OF THIOL-DISULFIDE BALANCE IN PARKINSON’S DISEASEКанунниковаН. П.KanunnikavaNina P.

д-р биол. наук, доцент, вед. науч. сотрудник

БЛК, 50, 230030, г. Гродно

D. Sc. (Biol.), Assistant Professor, Leading researcher

50, BLK, 230030, Grodno

n.kanunnikava@gmail.comИнститут биохимии биологически активных соединений НАН БеларусиInstitute of Biochemistry of Biologically Active Substances of the National Academy of Sciences of Belarus201804032018151108118Copyright © Канунникова Н.П., 20182018Канунникова Н.П.Kanunnikava N.P.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://vestimed.belnauka.by/jour/article/view/420

Болезнь Паркинсона (БП) является одной из наиболее распространенных нейродегенеративных патологий. Она характеризуется селективной гибелью ДА-нейронов в черной субстанции среднего мозга, обусловленной образованием избытка свободных радикалов и развитием окислительного стресса.

Попытки применения антиоксидантов как средств патогенетической терапии БП оказались безуспешными. Современные представления о развитии нейродегенеративных изменений при БП свидетельствуют о том, что важную роль в механизмах метаболических изменений, приводящих к гибели нейронов, играет не только усиление образования свободнорадикальных продуктов, но и недостаточная активность систем антиоксидантной защиты в ткани мозга. Важнейшими системами, участвующими в поддержании окислительно-восстановительного баланса в головном мозге, являются системы поддержания тиол-дисульфидного баланса, в частности система глутатиона (GSH/ GSSG), а также тиоредоксин, глутаредоксины, пероксиредоксин. В обзоре представлены данные, свидетельствующие о выраженных изменениях редокс-потенциала системы глутатиона, тиол-дисульфидного баланса, S-глутатионилирования белков в ткани мозга в экспериментальных моделях БП, а также в посмертных образцах ткани мозга пациентов с БП. Выяснение механизмов поддержания редокс-баланса в ткани мозга в условиях окислительного стресса при БП может послужить обоснованием для развития нового направления в нейропротекции и поиска новых средств патогенетической терапии БП. 

Parkinson’s disease (BP) is one of the most common neurodegenerative pathologies. It is characterized by a selective death of DA neurons in the black substance of the midbrain, resulting from the formation of an excess of free radicals and the development of oxidative stress.

Attempts to use antioxidants as a means of pathogenetic therapy of BP have been unsuccessful. Modern concepts of the understanding of the role of oxidative stress in the development of Parkinson’s disease (PD), as well as other neurodegenerative diseases suggest that an important role in the mechanisms of metabolic changes leading to the death of nervous tissue is played not only by the enhancement of formation of free radical products but also by the weakening of antioxidant defense systems in brain tissue. The most important components of the thiol/disulphide buffer systems involved in maintaining the redox balance in the brain are pairs of oxidized and reduced glutathione (GSH/GSSG), as well as thiol/disulfide oxidoreductases. Controlling the intensity of formation of free radical products from cellular antioxidant redox enzymes, primarily glutathione and thioredoxin-dependent enzyme systems, is extremely important not only to prevent brain tissue damage due to oxidative stress, but also to maintain the redox balance. The review presents the data showing pronounced changes in the redox potential of the glutathione system, thiol-disulphide balance, S-glutathionylation of in brain tissue proteins in experimental PD models, and in postmortem brain tissue samples of patients with PD. The elucidation of the mechanisms of maintaining the redox balance in brain tissue under oxidative stress in PD can serve as a justification for a new direction in neuroprotection and a search for new agents for pathogenetic therapy of PD. 

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The authors declare that there are no conflicts of interest present.