La3+, Gd3+ and Yb3+ induced changes in mitochondrial structure, membrane permeability, cytochrome c release and intracellular ROS level
La3+, Gd3+ and Yb3+ induced changes in mitochondrial structure, membrane permeability, cytochrome c release and intracellular ROS level
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DOI：
10.1016/s0009-2797(03)00072-3
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发表时间：
2003-07-25
影响因子：
5.1
通讯作者：
Wang, K
中科院分区：
文献类型：
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作者：
Liu, HX;Yuan, L;Wang, K
已知镧系元素 (Ln) 会诱导细胞凋亡，这可能是其对线粒体 (MT) 影响的结果。本研究试图阐明 NIT 和活性氧 (ROS) 在 Ln 诱导的细胞凋亡中的作用。我们发现微摩尔或更低浓度的La3+、Gd3+和Yb3+与NIT结合并诱导分离的MT膨胀； EGTA处理可以抑制该过程。此外，La3+、Gd3+和Yb3+增加了NIT膜的流动性并降低了NIT膜电位(DeltaPsi(m))。这些都是对MT渗透率转变孔隙张开结果的推断。通过免疫细胞化学监测与 Ln 离子孵育后细胞色素 c (Cyt-c) 从 MT 中的释放，然而，仅在细胞的胞质溶胶中观察到 Cyt-c 释放。与这些事件同时发生的是，在暴露于 Ln 的细胞中发现了更高水平的 ROS。有人提出，Ln 通过 NIT 途径诱导细胞凋亡，并且 ROS 很可能参与该机制。 (C) 2003 Elsevier Science Ireland Ltd. 保留所有权利。
Lanthanides (Ln) were known to induce cell apoptosis, which might be the results of their effects on mitochondria (MT). This study was trying to clarify the role of NIT and reactive oxygen species (ROS) in Ln-induced apoptosis. We found that micromolar or lower concentration of La3+, Gd3+ and Yb3+ bound to NIT and induced swelling of isolated MT; EGTA treatment can inhibit the process. In addition, La3+, Gd3+ and Yb3+ increased the NIT membrane fluidity and decreased the NIT membrane potential (DeltaPsi(m)). All these were inferred to the results of MT permeability transition pore opening. Release of cytochrome c (Cyt-c) from the MT upon incubation with Ln ions was monitored by immunocytochemistry, however, Cyt-c release was observed only in the cytosol of cells. In parallel with these events, there was a higher level of ROS found in the cells exposed to Ln. It was proposed that Ln-induced apoptosis via the NIT pathways and it was highly possible that ROS were involved in the mechanism. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.