Forums
BCL-2 and glutathione: alterations in cellular redox state that regulate apoptosis sensitivity

https://doi.org/10.1016/S0891-5849(99)00174-4Get rights and content
Under a Creative Commons license
open archive

Abstract

The importance of intracellular glutathione (GSH) in the pathology of disease, particularly cancer, has long been appreciated. However the ubiquitous nature of GSH has made it difficult to ascribe to a specific molecular mechanism in disease fulfillment. In addition, in all but a few cases, the underlying genetic regulation of the cellular redox state disrupted in disease has not been well described. Early identification of the importance of intracellular GSH to detoxification reactions has now led to investigating the potential importance that glutathione chemistry has on signal transduction and molecular regulation of cellular physiology. Here new relationships between the cellular redox state and the apoptotic regulatory protein BCL-2 will be described with emphasis on potential mechanisms by which GSH can alter cellular physiology in addition to its role in detoxification.

Keywords

Apoptosis
Glutathione
BCL-2
Channel Regulator
Glutathionylation
Gene expression
Free radicals

Abbreviations

GSH
glutathione
BCL
breakpoint cluster locus
HIV
human immunodeficiency virus
NF-κB
Nuclear Factor-kappa B
NAC
n-acetyl cysteine
PDTC
pyrolidine dithiocarbamate
NO
nitric oxide

Cited by (0)

1

The author received his Bachelors of Science degree in 1990 from the University of Texas at Austin. While in college, he spent two summers performing biomedical research at M.D. Anderson Cancer Center in the areas of medical physics and immunology. Based on these positive experiences the author entered the University of Texas Graduate School of Biomedical Science in 1991 and worked in the Department of Radiation Oncology studying the molecular and biochemical mechanisms of radiation-induced apoptosis. After receiving a Masters degree in Radiation Biology (1996) and a Doctorate in Cancer Biology (1998) the author joined the Herzenberg Laboratory in the Department of Genetics at Stanford University Medical School where he continues to pursue insights into the mechanisms of apoptosis and how these relate to disease pathology.

Copyright © 1999 Elsevier Science Inc. All rights reserved.