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In Vivo Regulation of Hepatic Glutathione Synthesis: Effects of Food Deprivation or Glutathione Depletion by Electrophilic Compounds

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Biological Reactive Intermediates—II

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 136))

Abstract

Glutathione traps reactive intermediates of compounds such as acetaminophen and prevents their covalent binding to tissue macromolecules and their hepatotoxicity (Mitchell et al., 1973). The availability of glutathione for conjugate formation is, therefore, a critical determinant of the toxicity of electrophilic drug metabolites capable of alkylating nucleophilic sites on vital hepatic molecules. Indeed, depletion of glutathione by diethyl maleate leads to a striking increase in the extent of liver injury caused by such drug metabolites (Potter et al., 1974).

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Lauterburg, B.H., Mitchel, J.R. (1982). In Vivo Regulation of Hepatic Glutathione Synthesis: Effects of Food Deprivation or Glutathione Depletion by Electrophilic Compounds. In: Snyder, R., et al. Biological Reactive Intermediates—II. Advances in Experimental Medicine and Biology, vol 136. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-0674-1_34

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  • DOI: https://doi.org/10.1007/978-1-4757-0674-1_34

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