Blog
About

0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Glutathione in liver diseases and hepatotoxicity.

      Molecular Aspects of Medicine

      physiology, Signal Transduction, Oxidative Stress, Oxidation-Reduction, metabolism, Mitochondria, Liver Diseases, Humans, Glutathione, Apoptosis, Animals

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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.

          Related collections

          Author and article information

          Journal
          10.1016/j.mam.2008.08.003
          18786561

          Comments

          Comment on this article