Физиологические изменения митохондрий при сахарном диабете и фармакологические подходы по их устранению

Изучено состояние перекисного окисления липидов (ПОЛ), дыхания и окислительного фосфорилирования, митохондриальной Са²⁺-зависимой поры (mPTP) и антирадикальной активности митохондрий печени крыс при диабете, индуцированном стрептозотоцином (STZ). Рассмотрены пути коррекции выявленных повреждений митохондриальных мембран с использованием полифенола госситана, выделенного из хлопчатника Gossypium hirsutum L. Показано, что скорость дыхания митохондрий печени в состояниях V3 и V4 при STZ-индуцированном диабете увеличивается, что выражается в значительном снижении коэффициентов дыхательного контроля (V3/V4) и фосфорилирования (ADP/O). Полученные данные свидетельствуют о том, что во время STZ-индуцированного диабета происходит разобщение дыхания и окислительного фосфорилирования. Показано, что в условиях STZ-индуцированного диабета скорость набухания митохондрий печени выше, чем у интактных крыс, что предполагает открытое состояние mPTP. Госситан нормализует динамику mPTP, снижая эффекты STZ на митохондрии печени. Пози тивное влияние госситана (пероральная доза составляет 10 мг/кг массы тела в течение 8 дней) может быть опосредовано также антиоксидантными свойствами в отношении ПОЛ.

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