РОЛЬ СИСТЕМЫ ГЛУТАТИОНА В ПОДДЕРЖАНИИ РЕДОКС-ГОМЕОСТАЗА И АНТИОКСИДАНТНОЙ ЗАЩИТЫ ПРИ ВОСПАЛИТЕЛЬНЫХ И ДЕГЕНЕРАТИВНО-ДИСТРОФИЧЕСКИХ ЗАБОЛЕВАНИЯХ ОРГАНА ЗРЕНИЯ
Аннотация
Цель. Провести анализ литературных источников и оценить роль, состояние антиоксидантной системы глутатиона при воспалительных и дегенеративно-дистрофических заболеваниях органа зрения. Материал и методы. Проанализированы источники отечественной и зарубежной литературы по проблеме окислительного стресса и антиоксидантной защиты, роли глутатиона при воспалительных и дегенеративно-дистрофических заболеваниях органа зрения с использованием научно-медицинских баз данных. Произведена оценка более 120 источников медицинской литературы за последние 15 лет, для научного анализа отобраны 50 публикаций. Результаты. Установлено, что окислительный стресс, в основе которого лежат патологические реакции свободнорадикального окисления, включая и процессы ПОЛ, играет ведущую роль в развитии воспалительных и дегенеративно-дистрофических заболеваний органа зрения. Ключевое звено в антиоксидантной защите тканей глаза – глутатионовая система, включающая сам глутатион (GSH) и глутатион-зависимые ферменты: глутатионпероксидазу (ГПО), глутатионредуктазу (ГР), глутатион-S-трансферазу (ГSТ). При воспалительных и дегенеративно-дистрофических процессах в глазу наблюдается снижение внутриклеточного пула глутатиона, нарушение баланса между его восстановленными и окисленными формами (GSH/GSSG). Выводы. Окислительный стресс имеет высокую корреляцию с воспалительным процессом и является важнейшим патогенетическим механизмом при воспалительных и дегенеративно-дистрофических заболеваниях глаза. Ключевая роль в антиоксидантной защите и поддержании редокс-гомеостаза тканей глаза принадлежит глутатионовой системе, включающей сам GSH и глутатион-зависимые ферменты (ГПО, ГР, ГSТ). При воспалительных и дегенеративно-дистрофических процессах в глазу наблюдается снижение внутриклеточного пула глутатиона (GSH), нарушение баланса между его восстановленными и окисленными формами (GSH/GSSG). Сдвиг данного равновесия существенно осложняет функционирование клетки, вплоть до апоптоза, играет роль пускового механизма в развитии множества патологических состояний, в том числе и заболеваний органа зрения.
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