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- W2068448907 abstract "Ischemia-reperfusion injury resulting from production of reactive oxygen intermediates is one of the most likely pathophysiologic causes of liver dysfunction after liver transplantation. Glutathione is an essential endogenous antioxidant, and N-acetylcysteine (NAC) is a nontoxic precusor of glutathione. The aim of the present study was to examine whether NAC administration protects against cold ischemia-reperfusion injury in the rat liver. An isolated perfused rat liver model subjected to prolonged hypothermic ischemia, 48-hour cold storage, and 120 minutes of reperfusion was employed. Administration of NAC 15 minutes before liver harvest significantly reduced concentrations of liver enzymes released into perfusate samples and significantly increased glutathione concentration in liver tissue specimens compared with those after administration of 5 % dextrose. A glutathione-depleted liver was produced with intraperitoneal injection of buthionine sulfoximine, an inhibitor of γ-glutamylcysteine synthetase, 2 hours before intraportal administration of either NAC or 5% dextrose. Administration of NAC also reduced concentrations of liver enzymes released into perfusate samples compared with those after 5 % dextrose injection. These results suggest that NAC administration reduces cold ischemiareperfusion injury in the rat liver by acting as a substrate for glutathione synthesis and also as a self-scavenger of reactive oxygen intermediates." @default.
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- W2068448907 date "1997-01-01" @default.
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- W2068448907 title "Pretreatment with N-Acetylcysteine Protects against Cold Ischemia/Reperfusion Injury in the Rat Liver" @default.
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- W2068448907 doi "https://doi.org/10.15369/sujms1989.9.141" @default.
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