Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis
Wenmin Huang , Dunhai Li
,
Yongding Liu
DOI:10.1016/j.jes.2014.06.032
Received October 30, 2013,Revised December 19, 2013, Accepted , Available online September 10, 2014
Volume 26,2014,Pages 1930-1935
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 (60 mg/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 (2 μmol/L, complex I inhibitor) and antimycin A (0.01 μmol/L, complex Ⅲ inhibitor), but not by thenoyltrifluoroacetone (5 μmol/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.
