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ГБОУ ВПО Первый МГМУ им. И.М.Сеченова Минздрава РФ
1. Окислительный стресс и связанное с ним перекисное окисление липидов, активация нейтрофилов и других видов лейкоцитов как клеточная основа воспалительного процесса [1, 13, 38, 46]. 2. Истощение запаса метионина и глутатиона, приводящее к усиленному синтезу цитокинов, в том числе a-фактора некроза опухоли и активации комплемента, что усиливает процессы воспаления [37, 46, 61, 70]. 3. Зависимое от концентрации вещества повреждение митохондрий с подавлением их мембранного потенциала, угнетением тканевого дыхания и разобщением процессов окисления и фосфорилирования [3, 43, 46, 66]. 4. Сочетание подавления и усиления активности ферментов семейства цитохрома Р-450 (CYP1A2, CYP2B6, CYP2C19 и CYP3A4/5) с образованием большого количества активных цитотоксических метаболитов [12, 25, 33, 39].
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