Redox regulation of apoptotic cell death
- 1 January 1998
- journal article
- review article
- Published by Wiley in BioFactors
- Vol. 8 (1-2) , 1-5
- https://doi.org/10.1002/biof.5520080101
Abstract
Apoptosis is a special form of cell death, which can be triggered by a variety of signals and pathophysiological conditions, including oxidative stress. Activation of members of the caspase family of cysteine proteases is a crucial event in the apoptotic death program. Being cysteine proteases, the caspases are sensitive to the redox status of the cell, and their activity is blocked by excessive oxidative stress. Thus, alterations of intracellular redox status may either trigger or block the apoptotic death program, depending on the severity of the oxidative stress.Keywords
This publication has 23 references indexed in Scilit:
- Suppression of Apoptosis by Nitric Oxide via Inhibition of Interleukin-1β–converting Enzyme (ICE)-like and Cysteine Protease Protein (CPP)-32–like ProteasesThe Journal of Experimental Medicine, 1997
- Mitochondrial control of apoptosisPublished by Elsevier ,1997
- Involvement of Cellular Proteolytic Machinery in ApoptosisBiochemical and Biophysical Research Communications, 1997
- Fas‐induced programmed cell death is mediated by a Ras‐regulated O2− synthesisImmunology, 1996
- Rapid and Specific Efflux of Reduced Glutathione during Apoptosis Induced by Anti-Fas/APO-1 AntibodyJournal of Biological Chemistry, 1996
- Reactive oxygen species and programmed cell deathTrends in Biochemical Sciences, 1996
- Reactive oxygen species and programmed cell deathTrends in Biochemical Sciences, 1996
- Oxidants in mitochondria: from physiology to diseasesBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1995
- Bcl-2 functions in an antioxidant pathway to prevent apoptosisCell, 1993
- N-Acetylcysteine: A New Approach to Anti-HIV TherapyAIDS Research and Human Retroviruses, 1992