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Acute phenoptosis: sudden death after a crisis, mediated by mitochondrial reactive oxygen species (ROS)тезисы доклада
Информация о цитировании статьи получена из
Web of Science
Дата последнего поиска статьи во внешних источниках: 27 мая 2015 г.
- Авторы: Zorov D., Plotnikov E., Silachev D., Pevzner I., Zorova L., Morosanova M., Jankauskas S., Chupyrkina A., Pulkova N., Babenko V., Zorov S.
- Сборник: FEBS Journal
- Серия: Special Issue: 38th FEBS Congress, Saint Petersburg, Russia, July 6–11, 2013
- Том: 280
- Тезисы
- Год издания: 2013
- Первая страница: 249
- Последняя страница: 250
- Аннотация: Mitochondria are multifunctional structures involved in a number of energy-producing and transducing processes and beyond these. Participation of mitochondria in cell death has received significant support while recent data point to their role in programmed organ failure and organismal death. The clearly programmed syndrome of multiple, simultaneous failure of a number of organs (MOF) is obviously a particular example and a source of phenoptotic death of a system. Histological examination often shows no signs of necrotic or apoptotic cell death in a failed tissue, however, signs of mitochondrial dysfunction have been repeatedly described. The mechanisms of mitochondriamediated phenoptosis may include generation of ROS and damage- associated molecular patterns (DAMPs) by mitochondria. DAMPs have been shown to mediate a fatal systemic inflammatory response syndrome caused by trauma through initial activation of innate immunity. Sepsis, a possible cause of MOF, was observed as the intermediate stage between the initial damage and MOF. However, in the syndrome of systemic inflammatory response observed in trauma or hemorrhagic shock the blood is sterile. The clinical picture of this phenomenon is not distinguishable from that of bacterial sepsis and mortality is very high in both cases. A unique role in a deadly cascade resulting in organism failure belongs to the kidney. It has been known that any pathology accompanied by acute renal failure increases mortality by 15–60%. In our experiments with rats when one of the two kidneys is removed and the remaining kidney is exposed to ischemia/ reperfusion, acute renal failure develops. However, in rats pre-treated with the mitochondria-targeted antioxidant SkQR1 the severity of renal failure is significantly reduced. In addition, the other mitochondrial antioxidant, SkQ1, did not improve renal function although both antioxidants almost completely abolished animal death which was as high as 70% in the absence of the antioxidants. We conclude that contrary to popular belief it was not renal failure that was the cause of animal death but some control system which is the target of used antioxidants. We speculate that it is the immune system involved in mitochondrial signaling that may be responsible for organismal death.
- Добавил в систему: Зорова Любава Дмитриевна