Glutathione in liver diseases and hepatotoxicity
Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H 2O 2 and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varie...
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| Published in | Molecular aspects of medicine Vol. 30; no. 1; pp. 29 - 41 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.02.2009
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0098-2997 1872-9452 1872-9452 |
| DOI | 10.1016/j.mam.2008.08.003 |
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| Abstract | Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H
2O
2 and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varied forms of oxidation, altering the function of signal transduction and transcription factor molecules. Increasing evidence supports the important role of ROS and GSH in modulating multiple signaling pathways. TNF-α and Fas signaling, NF-κB, JNK and mitochondrial apoptotic pathways are the focus of this review. The redox regulation either can switch on/off or regulate the threshold for some crucial events in these pathways. Notably, mitochondrial GSH depletion induces increased mitochondrial ROS exposure which impairs bioenergetics and promotes mitochondrial permeability transition pore opening which is critical for cell death. Depending on the extent of mitochondrial damage, NF-κB inhibition and JNK activation, hepatocytes may either undergo different modes of cell death (apoptosis or necrosis) or be sensitized to cell-death stimuli (i.e. TNF-α). These processes have been implicated in the pathogenesis of many liver diseases. |
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| AbstractList | Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H
2O
2 and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varied forms of oxidation, altering the function of signal transduction and transcription factor molecules. Increasing evidence supports the important role of ROS and GSH in modulating multiple signaling pathways. TNF-α and Fas signaling, NF-κB, JNK and mitochondrial apoptotic pathways are the focus of this review. The redox regulation either can switch on/off or regulate the threshold for some crucial events in these pathways. Notably, mitochondrial GSH depletion induces increased mitochondrial ROS exposure which impairs bioenergetics and promotes mitochondrial permeability transition pore opening which is critical for cell death. Depending on the extent of mitochondrial damage, NF-κB inhibition and JNK activation, hepatocytes may either undergo different modes of cell death (apoptosis or necrosis) or be sensitized to cell-death stimuli (i.e. TNF-α). These processes have been implicated in the pathogenesis of many liver diseases. Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H(2)O(2) and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varied forms of oxidation, altering the function of signal transduction and transcription factor molecules. Increasing evidence supports the important role of ROS and GSH in modulating multiple signaling pathways. TNF-alpha and Fas signaling, NF-kappaB, JNK and mitochondrial apoptotic pathways are the focus of this review. The redox regulation either can switch on/off or regulate the threshold for some crucial events in these pathways. Notably, mitochondrial GSH depletion induces increased mitochondrial ROS exposure which impairs bioenergetics and promotes mitochondrial permeability transition pore opening which is critical for cell death. Depending on the extent of mitochondrial damage, NF-kappaB inhibition and JNK activation, hepatocytes may either undergo different modes of cell death (apoptosis or necrosis) or be sensitized to cell-death stimuli (i.e. TNF-alpha). These processes have been implicated in the pathogenesis of many liver diseases.Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H(2)O(2) and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varied forms of oxidation, altering the function of signal transduction and transcription factor molecules. Increasing evidence supports the important role of ROS and GSH in modulating multiple signaling pathways. TNF-alpha and Fas signaling, NF-kappaB, JNK and mitochondrial apoptotic pathways are the focus of this review. The redox regulation either can switch on/off or regulate the threshold for some crucial events in these pathways. Notably, mitochondrial GSH depletion induces increased mitochondrial ROS exposure which impairs bioenergetics and promotes mitochondrial permeability transition pore opening which is critical for cell death. Depending on the extent of mitochondrial damage, NF-kappaB inhibition and JNK activation, hepatocytes may either undergo different modes of cell death (apoptosis or necrosis) or be sensitized to cell-death stimuli (i.e. TNF-alpha). These processes have been implicated in the pathogenesis of many liver diseases. Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H(2)O(2) and scavenging reactive oxygen and nitrogen radicals. In addition, GSH-induced redox shift with or without ROS subjects some cellular proteins to varied forms of oxidation, altering the function of signal transduction and transcription factor molecules. Increasing evidence supports the important role of ROS and GSH in modulating multiple signaling pathways. TNF-alpha and Fas signaling, NF-kappaB, JNK and mitochondrial apoptotic pathways are the focus of this review. The redox regulation either can switch on/off or regulate the threshold for some crucial events in these pathways. Notably, mitochondrial GSH depletion induces increased mitochondrial ROS exposure which impairs bioenergetics and promotes mitochondrial permeability transition pore opening which is critical for cell death. Depending on the extent of mitochondrial damage, NF-kappaB inhibition and JNK activation, hepatocytes may either undergo different modes of cell death (apoptosis or necrosis) or be sensitized to cell-death stimuli (i.e. TNF-alpha). These processes have been implicated in the pathogenesis of many liver diseases. |
| Author | Kaplowitz, Neil Yuan, Liyun |
| Author_xml | – sequence: 1 givenname: Liyun surname: Yuan fullname: Yuan, Liyun organization: Internal Medicine, University of Southern California, USA – sequence: 2 givenname: Neil surname: Kaplowitz fullname: Kaplowitz, Neil email: kaplowit@usc.edu organization: USC Research Center for Liver Diseases, University of Southern California, Keck School of Medicine, 2011, Zonal Avenue, 101, Los Angeles, CA 90033, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18786561$$D View this record in MEDLINE/PubMed |
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| Keywords | Signaling pathways Oxidative stress Mitochondria Redox Alcohol Hepatotoxicity Glutathione Apoptosis Necrosis |
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| Snippet | Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H
2O
2 and... Glutathione (GSH) is a major antioxidant as well as redox and cell signaling regulator. GSH guards cells against oxidative injury by reducing H(2)O(2) and... |
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| SubjectTerms | Alcohol Animals Apoptosis Apoptosis - physiology Glutathione Glutathione - metabolism Glutathione - physiology Hepatotoxicity Humans Liver Diseases - metabolism Mitochondria Mitochondria - metabolism Necrosis Oxidation-Reduction Oxidative stress Oxidative Stress - physiology Redox Signal Transduction - physiology Signaling pathways |
| Title | Glutathione in liver diseases and hepatotoxicity |
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