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

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(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 ofΔΨm.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.