Skip Navigation



Carcinogenesis Advance Access published online on April 13, 2007
Carcinogenesis, doi:10.1093/carcin/bgm093
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
28/10/2166    most recent
bgm093v2
bgm093v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Cox, A. G.
Right arrow Articles by Hampton, M. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cox, A. G.
Right arrow Articles by Hampton, M. B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Bcl-2 overexpression promotes genomic instability by inhibiting apoptosis of cells exposed to hydrogen peroxide

Andrew G. Cox1,2 and Mark B. Hampton1

1 Free Radical Research Group, Department of Pathology, Christchurch School of Medicine & Health Sciences, University of Otago, Christchurch, New Zealand
2 School of Biological Sciences, University of Canterbury, Christchurch, New Zealand

Corresponding author: Dr Mark Hampton, Department of Pathology, Christchurch School of Medicine & Health Sciences, PO Box 4345, Christchurch, New Zealand, Tel: + 64 3 364 1524, Fax: + 64 3 364 1083, E-mail: mark.hampton{at}chmeds.ac.nz

The anti-apoptotic oncogene bcl-2 is hypothesised to increase the antioxidant status of cells, thereby protecting them from oxidative stress. In this study we examined H2O2-mediated oxidative stress in Jurkat T lymphoma cells. Overexpression of Bcl-2 did not inhibit cytotoxicity at doses of H2O2 that caused necrosis (> 200 µM), but it did block cell death at apoptotic doses (< 200 µM). However, these cells exhibited the same initial level of protein and lipid oxidation following exposure to H2O2 as the parental cells, indicating that the anti-apoptotic activity is not associated with general antioxidant properties. Bcl-2 expression was able to protect against secondary protein carbonyl formation, which was linked to lysosome stabilization. Assessment of micronuclei formation in cells overexpressing Bcl-2 showed evidence of increased genomic instability, consistent with the impairment of apoptosis in damaged cells. We conclude that while Bcl-2 can block cytotoxicity associated with apoptosis-inducing levels of oxidative stress, it does not protect the cells from the stress itself. Bcl-2 may promote tumourigenesis by preventing the removal of oxidatively damaged cells.

Key Words: oxidative stress • apoptosis • micronuclei

Received December 21, 2006; revised April 3, 2007; accepted April 4, 2007.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
K. Chitcholtan, M. B. Hampton, and J. I. Keenan
Outer membrane vesicles enhance the carcinogenic potential of Helicobacter pylori
Carcinogenesis, December 1, 2008; 29(12): 2400 - 2405.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.