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

Abstract

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.

• Authors: Wenmin Huang, Dunhai Li, Yongding Liu
• Journal: Journal of environmental sciences (China) (J Environ Sci (China)) Vol. 26 Issue 9 Pg. 1930-5 (Sep 01 2014) ISSN: 1001-0742 [Print] Netherlands
• PMID: 25193844 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2014. Published by Elsevier B.V.

Chemical References

• Marine Toxins
• Microcystins
• microcystin RR

Topics

• Apoptosis (drug effects)
• Cell Line
• Electron Transport (drug effects)
• Marine Toxins
• Microcystins (toxicity)
• Mitochondria (drug effects)
• Tobacco