Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis

作     者：Wenmin Huang Dunhai Li Yongding Liu 

作者机构：Key Laboratory of Algal BiologyInstitute of HydrobiologyChinese Academy of Sciences Key Laboratory of Aquatic Botany and Watershed EcologyWuhan Botanical Gardenthe Chinese Academy of Sciences 

出 版 物：《Journal of Environmental Sciences》 (环境科学学报（英文版）)

年 卷 期：2014年第26卷第9期

页      面：1930-1935页

核心收录：

学科分类：0830[工学-环境科学与工程（可授工学、理学、农学学位）] 07[理学] 09[农学] 0903[农学-农业资源与环境] 0713[理学-生态学] 

基　　金：supported by the National Natural Science Foundation of China (No.31100340) the Major Science and Technology Program for Water Pollution Control and Treatment (No.2012ZX07103-004-02) 

主　　题：Microcystin RRTobacco BY 2 cellsApoptosisReactive oxygen speciesMitochondrial electron transport chain 

摘      要：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 . 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 （60 mg/L） displayed apoptotic changes in association with an increased production of ROS and loss of Am. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone （2 μmol/L, complex I inhibitor） and antimycin A （0.01 μmol/L, complex III inhibitor）, but not by thenoyltrifluoroacetone （S μmol/L, complex Ⅱinhibitor）. These results suggest that rnitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.