ИЗМЕНЕНИЯ ТИОЛ-ДИСУЛЬФИДНОГО БАЛАНСА ПРИ БОЛЕЗНИ ПАРКИНСОНА

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. 

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