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Oxidative Upregulation of Bcl-2 in Healthy Lymphocytes

Authors
Type
Published Article
Journal
Annals of the New York Academy of Sciences
Publisher
Wiley (Blackwell Publishing)
Publication Date
Dec 24, 2006
Volume
1091
Issue
1
Pages
9–9
Identifiers
DOI: 10.1196/annals.1378.049
Source
LBMCC
Keywords
License
Yellow

Abstract

In many cell systems, pharmacological glutathione (GSH) depletion with the GSH neosynthesis inhibitor buthionine sulfoximine (BSO) leads to cell death and highly sensitizes tumor cells to apoptosis induced by standard chemotherapeutic agents. However, some tumor cells upregulate Bcl-2 in response to BSO, thus surviving the treatment and failing to be chemosensitized. Cell lines of monocytic and lymphocytic origins respond to BSO treatment in an opposite way, lymphocytes being chemosensitized and unable to transactivate Bcl-2. In this article we investigate the response to BSO of lymphocytes freshly isolated from peripheral blood of healthy donors. After ensuring that standard separation procedures do not alter per se lymphocytes redox equilibrium nor Bcl-2 levels in the first 24 h of culture, we show that BSO treatment promotes the upregulation of Bcl-2, with a mechanism involving the increased radical production consequent to GSH depletion. Thus, BSO treatment may increase the differential cytocidal effect of cytotoxic drugs in tumor versus normal lymphocytes.

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