Expression of BCL-2 Inhibits Cellular Radical Generation

Martina Wiedau-Pmos Department of Neurology, Brain Research Institutet, Molecular Biology Institute and Jules Stein Eye Institutet, University of Calfornia, Los Angeles, CA, 90024–1769, USA; Department of Anesthesia, Stunford University School of Mediane, Stanford, CA, 94305, USA

James R. Trudell Department of Neurology, Brain Research Institutet, Molecular Biology Institute and Jules Stein Eye Institutet, University of Calfornia, Los Angeles, CA, 90024–1769, USA; Department of Anesthesia, Stunford University School of Mediane, Stanford, CA, 94305, USA

Christian Altenbach Department of Neurology, Brain Research Institutet, Molecular Biology Institute and Jules Stein Eye Institutet, University of Calfornia, Los Angeles, CA, 90024–1769, USA; Department of Anesthesia, Stunford University School of Mediane, Stanford, CA, 94305, USA

Darci J. Kane Department of Neurology, Brain Research Institutet, Molecular Biology Institute and Jules Stein Eye Institutet, University of Calfornia, Los Angeles, CA, 90024–1769, USA; Department of Anesthesia, Stunford University School of Mediane, Stanford, CA, 94305, USA

Wayne L. Hubbell Department of Neurology, Brain Research Institutet, Molecular Biology Institute and Jules Stein Eye Institutet, University of Calfornia, Los Angeles, CA, 90024–1769, USA; Department of Anesthesia, Stunford University School of Mediane, Stanford, CA, 94305, USA

Dale E. Bredesen Department of Neurology, Brain Research Institutet, Molecular Biology Institute and Jules Stein Eye Institutet, University of Calfornia, Los Angeles, CA, 90024–1769, USA; Department of Anesthesia, Stunford University School of Mediane, Stanford, CA, 94305, USA

Abstract

Bcl-2 expression in neural cells has been shown to inhibit apoptotic death in association with a decrease in reactive oxygen species. We present the results of a study that used electron spin resonance (ESR) measurements to evaluate the level of hydroxyl radical production in bcl-2 expressing GT1–7 cells and control cells. Incubation of cell monolayers with the spin trap N-t-α-phenylnitrone (PBN), and measurement of the hydroxyl radical production at different timepoints, revealed a higher radical production in control cells than in bcl-2 expressing cells, even in the absence of insult. The ESR signal was suppressed by addition of ethanol, indicating that the trapped radical was indeed hydroxyl radical. The mechanism by which the expression of bcl-2 leads to a decrease in cellular production of hydroxyl radical is unknown.

Key Words:

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Order Reprints Request Corporate Permissions

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

Request Academic Permissions

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.

Expression of BCL-2 Inhibits Cellular Radical Generation

Information for

Open access

Opportunities

Help and information

Expression of BCL-2 Inhibits Cellular Radical Generation

Abstract

Reprints and Corporate Permissions

Academic Permissions

Related research

To cite this article:

Download citation

Information for

Open access

Opportunities

Help and information

Keep up to date

Your download is now in progress and you may close this window

Login or register to access this feature