https://scholars.lib.ntu.edu.tw/handle/123456789/194437
標題: | 粒線體功能異常對人體神經細胞的影響(2/2) | 作者: | 李旺祚 | 關鍵字: | 3-nitropropionic acid;mitochondrial permeability transition;caspase;antioxidant;apoptosis;NMDA-GIuR;NMDA 受體;鈣離子;內質網 | 公開日期: | 2002 | 出版社: | 臺北市:國立臺灣大學醫學院小兒科 | 摘要: | 3-Nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase, induced ATP depletion and both necrosis and apoptosis in human NT2-N neurons. Necrosis occurred predominantly during the first 2 days in a dose-dependent manner, whereas apoptosis was observed after 24 hr or later at a low constant rate in 0.1mM as well as 5mM 3-NP. We assayed the intracellular concentration of Ca24- ([Ca2j1) during the first 48 hours in 1mM 3-NP, a period during which 10% of the neurons died by necrosis and 3% by apoptosis. During the first 2 hours in 3-NP, all NT2-N neurons showed [Ca2j1 rise from48¡Ó2 to 140¡Ó l2nM(mean¡ÓSEM¡¦). After 24 and 48 hours in 3-NP, however, [Ca24-J remained above IOOnM in only 17% and 25% of the NT2-N neurons, respectively, suggesting that most neurons were able to correct this early rise in [Ca24-], despite severe ATP depletion, and to survive. Activation of NMDA-GIuR contributed substantially to 3-NP-induced ATP depletion, and subsequent chronic elevation of [Ca24-]1 in the NT2-N neurons. We also demonstrated that blocking endoplasmic reticulum (ER) Ca24- release enhanced the capacity of these human neurons to maintain [Ca21], homeostasis and resist necrosis while subjected to chronic energy deprivation. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/22874 | 其他識別: | 902314B002183 | Rights: | 國立臺灣大學醫學院小兒科 |
顯示於: | 醫學系 |
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