Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 37, Issue 10, Pages 1511-1526Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2004.06.040
Keywords
cysteine; glutathione; glutamate cysteine ligase; gamma-glutamylcysteine synthetase; gamma-glutamyltransferase; oxidative stress; redox regulation; thiol-disulfide exchange; free radicals
Funding
- NIA NIH HHS [R01 AG09235] Funding Source: Medline
- NIEHS NIH HHS [P30 ES06096, R01-ES012463, R01 ES10133] Funding Source: Medline
Ask authors/readers for more resources
The tripeptide glutathione (GSH) is part of an integrated antioxidant system that protects cells and tissues from oxidative damage. Oxidative stress can result from exposure to excessive amounts of endogenous and exogenous electrophiles. Until recently, animal and cell model systems used to investigate the role of GSH in disease processes had employed chemical agents that deplete cellular GSH by inhibiting GSH synthesis or by reacting chemically with GSH. Such models have proven useful, but questions concerning nonspecific effects of such chemicals remain. Recently, our laboratories and others have developed mouse models with genetic deficiencies in enzymes of the GSH biosynthetic pathway. This review focuses on the regulation of GSH homeostasis and, specifically, the new GSH-deficient mouse models that have been developed. These models will improve our understanding of the role of GSH in animal and human diseases. (C) 2004 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available