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• W1600359323 abstract "This chapter provides a brief background in glutathione function metabolism and discusses currently available methods for increasing cellular glutathione levels. Glutathione (γ-glutamylcysteinylglycine; GSH) is the major cellular antioxidant and is found in high concentrations in most mammalian cells. GSH has several functions, including roles in metabolism, transport, catalysis (coenzyme), and maintenance of the thiol moieties of proteins and the reduced form of other molecules such as cysteine, coenzyme A, and antioxidants such as ascorbic acid; it is also used in the formation of deoxyribonucleic acids. GSH participates in the protection against toxic compounds. One of its important functions is in the protection against oxidative damage caused by reactive oxygen species (ROS), many of which are generated during normal metabolism. GSH can react nonenzymatically with ROS, and GSH peroxidase (and non-Se peroxidase) catalyzes the destruction of hydrogen peroxide and hydroperoxides. γ-Glutamylcysteine synthetase is nonallosterically feedback inhibited by GSH. The degradation of the γ-glutamyl moiety of GSH (or GSH S-conjugates) is catalyzed by γ-glutamyl transpeptidase, a membrane-bound enzyme whose active site is on the external surface of certain cells. GSH is normally transported out of cells where transpeptidation occurs in the presence of amino acids, and a γ-glutamyl amino acid is formed. This can then be transported into cells where it, but not GSH, is a substrate for γ -glutamyl cyclotransferase and forms amino acid and 5-oxoproline. 5-Oxoproline is ring opened by 5-oxoprolinase to form glutamate. The chapter discusses the various GSH deficiencies that include inborn error of metabolism, l-Buthionine-SR-Sulfoximine (BSO)-induced GSH deficiency, and disease associated with oxidative damage. The discussion includes the glutathione delivery compounds with l-2-Oxothiazolidine-4-Carboxylic Acid, γ-Glutamylcyst(e)ine, Glutathione Monoesters and GSH Diester. The several methods for modulating cellular GSH levels presented in this chapter offer selective tools to study mechanisms and offer potential therapy of human diseases associated with GSH deficiency and oxidative stress." @default.
• W1600359323 created "2016-06-24" @default.
• W1600359323 creator A5015017352 @default.
• W1600359323 date "1996-01-01" @default.
• W1600359323 modified "2023-10-18" @default.
• W1600359323 title "Glutathione and Glutathione Delivery Compounds" @default.
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• W1600359323 doi "https://doi.org/10.1016/s1054-3589(08)60979-5" @default.
• W1600359323 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8895804" @default.
• W1600359323 hasPublicationYear "1996" @default.
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