Decreased hepatic glutathione levels in septic shock. Predisposition of hepatocytes to oxidative stress: an experimental approach.
Intracellular metabolite glutathione, existing in either its reduced (GSH) or oxidized states, is crucial for the protection of any cell against an oxidative stress or injury. Significant depletion of intracellular levels of GSH predisposes cells to an oxidative injury. We have investigated the level of hepatic GSH during the early course of sepsis in a physiologically well-characterized septic-sheep model. Following six hours of sepsis, which was characterized by hypotension, hypoxemia, and granulocytopenia, the level of intrahepatic GSH was significantly reduced compared with baseline levels. There was no reduction after two hours of sepsis. Hepatic GSH levels in control animals were unchanged compared with baseline levels. These findings suggest that the liver may be more susceptible to an oxidative stress in septic patients.
D000818:Animals; D019328:Buthionine Sulfoximine; D002478:Cells, Cultured; D004927:Escherichia coli Infections / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D005978:Glutathione / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008099:Liver / Q000378:metabolism*; D008111:Liver Function Tests; D008717:Methionine Sulfoximine / Q000031:analogs & derivatives / Q000494:pharmacology; D009102:Multiple Organ Failure; D010084:Oxidation-Reduction; D014176:Protein Biosynthesis; D012756:Sheep; D012772:Shock, Septic / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology
D008717:Methionine Sulfoximine; D019328:Buthionine Sulfoximine; D006861:Hydrogen Peroxide; D005978:Glutathione