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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 486267, 7 pages
Research Article

The Protection of Hepatocyte Cells from the Effects of Oxidative Stress by Treatment with Vitamin E in Conjunction with DTT

1Department of Physical Therapy, School of Medical and Health Sciences, Fooyin University, Kaohsiung 83102, Taiwan
2School of Nutrition and Institute of Nutrition, College of Health Care, China Medical University, Taichung 40402, Taiwan
3School of Nutrition, College of Health Care and Management, Chung Shan Medical University, Taichung 40203, Taiwan
4Graduate Institute of Cancer Biology, College of Medicine, China Medical University, Taichung 40402, Taiwan
5Center for Molecular Medicine, College of Medicine, China Medical University, Taichung 40402, Taiwan

Received 16 November 2009; Accepted 25 March 2010

Academic Editor: George E. Plopper

Copyright © 2010 Jen-Hsiang Tsai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We investigated the effect of vitamin E on membrane protein thiols under oxidative stress, which we induced by treating hepatocytes with tert-butyl hydroperoxide (TBH) for 60 mins. Those cells which we pretreated with vitamin E formed fewer blebs (22.3% compared to 60.0% in nonvitamin E-treated cells) and maintained cytosolic calcium concentration and the number of membrane protein thiols instead of showing the usual symptoms in cells undergoing oxidative stress. Dithiothreitol (DTT) also commonly reduces bleb formation in hepatocytes affected by TBH. However, our experiments clearly demonstrate that DTT does not prevent the changes in cytosolic calcium and membrane protein thiols in the blebbing cells. Consequently, we decided to pretreat cells with both DTT and vitamin E and found that the influence of TBH was entirely prevented. These findings may provide us with a new aspect for investigating the mechanism of bleb formation under oxidative stress.