Роль глутаматных рецепторов и энергетического обмена в токсичности аммиака

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Диссертация
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Биохимия
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102


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ам. миака, глутамата и глутамина в сердце (Davidson Sonnenblick, 1975). Кроме того, показано, что перфузия изолированного сердца хлоридом ам. мония (2,06 ммоль/л) увеличивает уровень аммиака до 4 мМ, но при этом не происходит ослабление сократимости сердца. Вильсон с сотрудниками изучали влияние токсических доз аммиака на лабораторных жшотных и обнаружил, что внутрибрюшинное введение ацетата аммония немедленно приводило к фибрилляции желудочков сердца у собак и овец (Wilson et al., 1964). Гибель животных при пшераммонемии связана с нарушением сердечной деятельности, а следовательно, токсическое действие аммиака может распространяется на миоциты. Нарушения энергетического обмена могут быть причинами развития дегенеративных процессов в мьппечных клетках сердца и ухудшения функции миоцитов при пшераммонемии. В отношении энергетического и любой иной формы обмена в сердце при пшераммонемии в настоящее время данных не имеется. О натичии NMDA-рецепторов в сердце Ж1тотных говорится всего в нескольких работах. Сибер с сотрудниками опредилили мРНК МК2В-субъединицы NMDA-рецептора и сам белок в сердечной ткани у эмбрионов крыс, но к 10-й неделе жизни животных субъединица NR2B не обнаруживатась (Seeber et al, 2000). В другой работе сообщатось о наливши мРНК белка NR1 в миоцитах крысы (Morhenn et al., 1994), Бьшо показано, что ММОЛ-рецепторы в клетках сердца обладают низким сродство. м к [Н]МК-801, и сделано предположение, что NRl-субъединица-возможно, общий «канат-образующий белок& raquo-, который присутствует во МИ0П1Х тканях и формирует специфические рецепторы, взаимодействуя с дополнительными субъединицами (Morhenn et al., 1994). 12 .9. Стационарные уровни аммиака в тканях Аммиак является важным клеточным метаболитом, участником по крайней мере 170 известных ферментативных реакций. Однако в высоких концентрациях он токсичен, особенно для нервной системы организма. Содержание

Результаты работы показали, что вводимая летальная доза аммиака не является токсичной для сердца. Сердце при сравнении с мозгом является более адаптивным органом в условиях гипераммонемии.

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Содержание

1. ОБЗОР ЛИТЕРАТУРНЫХ ДАННЫХ

1.1. Природа аммиака

1.2. Источники аммиака в организме

1.3. Выведение аммиака из организма

1.4. Цикл и биосинтез мочевины

1.5. Тканевое распределение ферментов цикла мочевины

1.6. Другие ферменты, тесно сопряженные с циклом мочевины

1.7. Обмен аммиака в мозге

1.8. Обмен аммиака в сердце

1.9. Стационарные уровни аммиака в тканях

1. 10. Нарушения в обмене аммиака. Гипераммонемия

1. 11. Причины гипераммонемии

1. 12. Токсичность аммиака

1. 13. Влияние аммиака на энергетический обмен

1. 14. Окислительный стресс при действии аммиака

1. 15. Действие гипераммонемии на глутаматные рецепторы

1. 16. Гипераммонемия, NMDA-рецепторы и перекисные процессы

1. 17. NMDA-рецепторы и гомеостаз кальция

1. 18. Аммиак, NMDA-рецепторы и энергетический обмен в клеточном ядре

1. 19. Цель и задачи исследования

2. МАТЕРИАЛЫ И МЕТОДЫ ИССЛЕДОВАНИЯ

3. РЕЗУЛЬТАТЫ РАБОТЫ

3.1. Концентрация аммиака в тканях при острой аммиачной интоксикации

3.2. Влияние аммиака на ферменты, участвующие в обмене аммиака

3.3. Влияние аммиака на окислительное фосфорилирование

3.4. Влияние аммиака на содержание адениновых нуклеотидов

3.5. Действие аммиака на транспорт кальция в несинаптических митохондриях мозга крысы

3.6. Роль аммиака в развитии окислительного стресса

3.7. Поли (АДФ-рибозо)полимераза, НАД-синтетаза, НАД-гликогидролаза, уровень НА/Г и супероксидного радикала в ядрах мозга при гипераммонемии

4. ВЫВОДЫ

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