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eCAM Advance Access published online on July 10, 2009
eCAM, doi:10.1093/ecam/nep082
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© 2009 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Bufalin Induces Reactive Oxygen Species Dependent Bax Translocation and Apoptosis in ASTC-a-1 Cells

Lei Sun1, Tongsheng Chen1, Xiaoping Wang2, Yun Chen3 and Xunbin Wei3

1MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, South China Normal University, Guangzhou, 510631,2Department of Anesthesiology, The First Affiliated Hospital of Jinan University, Guangzhou, 510632, China and 3Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, PR China

Bufalin has been shown to induce cancer cell death through apoptotic pathways. However, the molecular mechanisms are not well understood. In this study, we used the confocal fluorescence microscopy (CFM) to monitor the spatio-temporal dynamics of reactive oxygen species (ROS) production, Bax translocation and caspase-3 activation during bufalin-induced apoptosis in living human lung adenocarcinoma (ASTC-a-1) cells. Bufalin induced ROS production and apoptotic cell death, demonstrated by Hoechst 33258 staining as well as flow cytometry analysis. Bax redistributed from cytosol to mitochondria from 12 to 48 h after bufalin treatment in living cells expressed with green fluorescent protein Bax. Treatment with the antioxidant N-acetyl-cysteine (NAC), a ROS scavenger, inhibited ROS generation and Bax translocation and led to a significant protection against bufalin-induced apoptosis. Our results also revealed that bufalin induced a prominent increase of caspase-3 activation blocked potently by NAC. Taken together, bufalin induced ROS-mediated Bax translocation, mitochondrial permeability transition and caspase-3 activation, implying that bufalin induced apoptosis via ROS-dependent mitochondrial death pathway in ASTC-a-1 cells.

Keywords: N-acetyl-cysteine – Bax translocation – caspase-3 activation – fluorescence resonance energy transfer – mitochondrial dysfunction

For reprints and all correspondence: Tongsheng Chen and Xunbin Wei, Institute of Laser Life Science, South China Normal University, Guangzhou 510631, China, Tel: +86-20-85211436. Ext: 8606; Fax: +86-20-85216052; E-mail: chentsh{at}scnu.edu.cn

Received February 1, 2009; accepted June 15, 2009


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