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lipid hydroperoxides) as well as increased plasma endotoxin concentrations.27 In a previous study we have investigated the intestinal epithelial barrier function in patients with compensated liver cirrhosis in order to find out whether an increased intestinal permeability may be a risk factor for the progression towards decompensated cirrhosis and observed an increased small intestinal permeability in a subgroup of patients with alcohol-related cirrhosis and an increased large intestinal permeability in the whole group of compensated cirrhotic patients.28 We hypothesized that intestinal oxidative stress is involved in the epithelial barrier dysfunction of patients with compensated liver cirrhosis

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In mice, a null mutation in the gene encoding one subunit of GCS was found to be embryonic lethal

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