线粒体电子传递链参与微囊藻毒素-RR 诱导的烟草 BY-2 细胞凋亡。
Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis.
机构信息
Key Laboratory of Algal Biology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China; Key Laboratory of Aquatic Botany and Watershed Ecology, Wuhan Botanical Garden, the Chinese Academy of Sciences, Wuhan 430074, China.
Key Laboratory of Algal Biology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China.
出版信息
J Environ Sci (China). 2014 Sep 1;26(9):1930-5. doi: 10.1016/j.jes.2014.06.032. Epub 2014 Jul 9.
Microcystin-RR (MC-RR) has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential (ΔΨm). To further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain (ETC) as a potential source for reactive oxygen species (ROS). Tobacco BY-2 cells after exposure to MC-RR (60mg/L) displayed apoptotic changes in association with an increased production of ROS and loss of ΔΨm. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone (2μmol/L, complex I inhibitor) and antimycin A (0.01μmol/L, complex III inhibitor), but not by thenoyltrifluoroacetone (5μmol/L, complex II inhibitor). These results suggest that mitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.
微囊藻毒素-RR（MC-RR）已被证明通过线粒体功能障碍，包括线粒体膜电位（ΔΨm）的丧失，诱导烟草 BY-2 细胞凋亡。为了进一步阐明 MC-RR 诱导烟草 BY-2 细胞凋亡的机制，我们研究了线粒体电子传递链（ETC）作为活性氧（ROS）潜在来源的作用。暴露于 MC-RR（60mg/L）的烟草 BY-2 细胞显示出与 ROS 产生增加和 ΔΨm 丧失相关的凋亡变化。所有这些不良反应都被 ETC 抑制剂（包括 Rotenone（2μmol/L，复合物 I 抑制剂）和 Antimycin A（0.01μmol/L，复合物 III 抑制剂））显著减轻，但不被 2,4-二硝基苯酚（5μmol/L，复合物 II 抑制剂）减轻。这些结果表明，线粒体 ETC 通过增加线粒体 ROS 的产生，在介导 MC-RR 诱导的烟草 BY-2 细胞凋亡中起关键作用。
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