HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 291/1/G1    most recent 00001.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (15) Citing Articles via Google Scholar Google Scholar Articles by Han, D. Articles by Kaplowitz, N. Search for Related Content PubMed PubMed Citation Articles by Han, D. Articles by Kaplowitz, N.

THEME

Mechanisms of Liver Injury. III. Role of glutathione redox status in liver injury

University of Southern California (USC) Research Center for Liver Diseases, USC-University of California-Los Angeles Research Center for Alcohol Liver and Pancreatic Diseases, Keck School of Medicine, USC, Los Angeles, California

Submitted 4 January 2006 ; accepted in final form 6 February 2006

GSH is the most abundant redox molecule in cells and thus the most important determinant of cellular redox status. Thiols in proteins can undergo a wide range of reversible redox modifications (e.g., S-glutathionylation, S-nitrosylation, and disulfide formation) during times of increased exposure to reactive oxygen and nitrogen species, which can affect protein activity. These reversible thiol modifications regulated by GSH may be nanoswitches to turn on and off proteins, similar to phosphorylation, in cells. In the cytoplasm, an altered redox state can activate (e.g., MAPKs and NF-E2-related factor-2) and inhibit (e.g., phosphatases and caspases) proteins, whereas in the nucleus, redox alterations can inhibit DNA binding of transcription factors (e.g., NF-B and activator protein-1). The consequences include the promotion of expression of antioxidant genes and alterations of hepatocyte survival as well as the balance between necrotic versus apoptotic cell death. Therefore, the understanding of the redox regulation of proteins may have important clinical ramifications in understanding the pathogenesis of liver diseases.

thiol; disulfide; S-glutathionylation

This article has been cited by other articles:

				N. Sayed, D. D. Kim, X. Fioramonti, T. Iwahashi, W. N. Duran, and A. Beuve Nitroglycerin-Induced S-nitrosylation and Desensitization of Soluble Guanylyl Cyclase Contribute to Nitrate Tolerance Circ. Res., September 12, 2008; 103(6): 606 - 614. [Abstract] [Full Text] [PDF]

				B. Saberi, M. Shinohara, M. D. Ybanez, N. Hanawa, W. A. Gaarde, N. Kaplowitz, and D. Han Regulation of H2O2-induced necrosis by PKC and AMP-activated kinase signaling in primary cultured hepatocytes Am J Physiol Cell Physiol, July 1, 2008; 295(1): C50 - C63. [Abstract] [Full Text] [PDF]