The effect of acute ethanol consumption on plasma glutathione (GSH) and malondialdehyde (MDA) concentrations was studied in two groups of healthy male subjects. The first group (n = 15) received an acute dose of ethanol (1.5 g/kg p.o. over a period of 3 h); in the control group (n = 15), ethanol was replaced isocalorically with carbohydrates. Blood samples were taken at 0 time (ethanol/carbohydrates ingestion) and every 60 min for 6 h. A significant increase in plasma MDA concentration as well as in plasma GSH values were observed in subjects receiving ethanol compared to controls. The enhancement of plasma GSH was accompanied by a concomitant increase of oxidized glutathione (GSSG). These data support the hypothesis of an increase of lipid peroxidation as a possible mechanism of acute ethanol toxicity. The enhancement of plasma GSH and GSSG may reflect an increased utilization and loss of the tripeptide from the liver induced by ethanol.

Increased plasma levels of glutathione and malondialdehyde after acute ethanol ingestion in humans.

VENDEMIALE, GIANLUIGI;
1989-01-01

Abstract

The effect of acute ethanol consumption on plasma glutathione (GSH) and malondialdehyde (MDA) concentrations was studied in two groups of healthy male subjects. The first group (n = 15) received an acute dose of ethanol (1.5 g/kg p.o. over a period of 3 h); in the control group (n = 15), ethanol was replaced isocalorically with carbohydrates. Blood samples were taken at 0 time (ethanol/carbohydrates ingestion) and every 60 min for 6 h. A significant increase in plasma MDA concentration as well as in plasma GSH values were observed in subjects receiving ethanol compared to controls. The enhancement of plasma GSH was accompanied by a concomitant increase of oxidized glutathione (GSSG). These data support the hypothesis of an increase of lipid peroxidation as a possible mechanism of acute ethanol toxicity. The enhancement of plasma GSH and GSSG may reflect an increased utilization and loss of the tripeptide from the liver induced by ethanol.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11369/118342
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