Inhibition of Axonal Transport Caused by tert-Butyl Hydroperoxide in Cultured Mouse Dorsal Root Ganglion Neurons
Inhibition of Axonal Transport Caused by tert-Butyl Hydroperoxide in Cultured Mouse Dorsal Root Ganglion Neurons
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叔丁基过氧化氢对培养小鼠背根神经节神经元轴突运输的抑制
DOI：
10.1007/s12031-010-9457-3
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发表时间：
2011
影响因子：
3.1
通讯作者：
T. Kawakami
中科院分区：
文献类型：
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作者：
R. Isonaka;H. Hiruma;T. Kawakami
活性氧（ROS）能够影响神经元细胞的功能和结构。在这里，我们使用视频增强显微镜研究了过氧化氢（H2O2）（ROS 之一）对培养的小鼠背根神经节神经元轴突运输的直接影响。用 H2O2 供体叔丁基氢过氧化物（TBHP；10 nM–1 mM）处理神经元，以时间和浓度依赖性方式抑制细胞器的顺行和逆行运动。 100 μM 和 1 mM 的 TBHP 使线粒体和溶酶体明显肿胀，并导致轴突运输完全且不可逆地停止。相比之下，即使在最高 TBHP 浓度 (1 mM) 下，细胞骨架结构也明显没有变化。通过燕尾苝衍生物荧光检测到的脂质过氧化物是由 TBHP 在质膜中产生的，在细胞器膜中的产生程度更高。 TBHP 诱导的轴突运输、脂质过氧化物产生和细胞器肿胀的抑制可通过 α-生育酚（维生素 E，1 mM）预处理来阻断。这些结果表明，H2O2 通过脂质过氧化以及细胞器的退行性变化抑制轴突运输。
Reactive oxygen species (ROS) are capable of affecting neuronal cell function and structure. Here, we investigated the direct effects of hydrogen peroxide (H2O2), one of the ROS, on axonal transport in cultured mouse dorsal root ganglion neurons using video-enhanced microscopy. Treatment of neurons with the H2O2 donor tert-butyl hydroperoxide (TBHP; 10 nM–1 mM) inhibited anterograde and retrograde movement of organelles in a time- and concentration-dependent manner. Mitochondria and lysosomes were clearly swollen by TBHP at 100 μM and 1 mM in association with complete and irreversible cessation of axonal transport. In contrast, cytoskeletal structures were apparently unchanged even at the highest TBHP concentration (1 mM). Lipid peroxides, detected by swallow-tailed perylene derivative fluorescence, were produced by TBHP in plasma membranes and more highly in organelle membranes. The TBHP-induced inhibition of axonal transport, lipid peroxide production, and organelle swelling were blocked by pretreatment with α-tocopherol (vitamin E, 1 mM). These results suggest that H2O2 inhibited axonal transport via lipid peroxidation along with degenerative changes in organelles.
影响因子：
10.4
作者：
通讯作者：
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HSP27 磷酸化介导的抗氧化应激诱导的肌动蛋白断裂和细胞死亡的抵抗力。
影响因子：
11.2
作者：
Huot,J;Houle,F;Spitz,DR;Landry,J
通讯作者：
Landry,J