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Roles of mitochondria-generated reactive oxygen species on X-ray-induced apoptosis in a human hepatocellular carcinoma cell line, HLEстатья
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 14 февраля 2019 г.
- Авторы: Indo H.P., Inanami O., Koumura T., Suenaga S., Yen H.C., Kakinuma S., Matsumoto K., Nakanishi I., St Clair W., St Clair D.K., Matsui H., Cornette R., Gusev O., Okuda T., Nakagawa Y., Ozawa T., Majima H.J.
- Журнал: Free Radical Research
- Том: 46
- Номер: 8
- Год издания: 2012
- Издательство: Taylor & Francis
- Местоположение издательства: United Kingdom
- Первая страница: 1029
- Последняя страница: 1043
- Аннотация: HLE, a human hepatocellular carcinoma cell line was transiently transfected with normal human MnSOD and MnSOD without a mitochondrial targeting signal (MTS). Mitochondrial reactive oxygen species (ROS), lipid peroxidation and apoptosis were examined as a function of time following 18.8 Gy X-ray irradiation. Our results showed that the level of mitochondrial ROS increased and reached a maximum level 2 hours after X-ray irradiation. Authentic MnSOD, but not MnSOD lacking MTS, protected against mitochondrial ROS, lipid peroxidation and apoptosis. In addition, the levels of mitochondrial ROS were consistently found to always correlate with the levels of authentic MnSOD in mitochondria. These results suggest that only when MnSOD is located in mitochondria is it efficient in protecting against cellular injuries by X-ray irradiation and that mitochondria are the critical sites of X-ray-induced cellular oxidative injuries.
- Добавил в систему: Гусев Олег Александрович