Liver lipid peroxidation and glutathione-related defence enzyme systems in mice treated with paracetamol.

Glutathione levels were found to be decreased while lipid peroxide levels were increased in total liver homogenates 6 h following paracetamol treatment (500 mg kg-1 i.p.).

The hepatic lipid peroxidation, copper and fibrosis in cholestatic rats.

Hepatic lipid peroxidation was shown to be stimulated in the livers of cholestatic rats with increased hydroxyproline levels. In another group, cholestatic rats were fed with a copper-supplemented diet to increase hepatic copper levels. Although liver copper concentrations increased about 16-fold in copper supplemented cholestatic rats compared to normally fed cholestatic rats, no change was observed either in hepatic lipid peroxidation or in hydroxyproline levels.

Ethanol-induced changes in lipid peroxidation and glutathione content in rat brain.

The effect of acute and chronic ethanol administration on brain lipid peroxide and glutathione levels was investigated in rats. Acute ethanol administration (5 g/kg, i.p.

Inhibition of NADPH-induced microsomal lipid peroxidation in the livers of cholestatic rats.

NADPH-induced microsomal lipid peroxidation was found to be significantly inhibited in the livers of cholestatic rats. In cholestasis, microsomal cholesterol content was increased while phospholipid content remained unchanged.

The effect of chronic ethanol ingestion on brain lipid peroxide and glutathione levels in rats.

Rat liver and brain lipid peroxide and glutathione levels were determined after chronic ethanol treatment. Although hepatic lipid peroxidation was significantly stimulated, we have failed to observe any change in brain lipid peroxide and glutathione levels of rats chronically treated with ethanol.

Stimulation of lipid peroxidation and impairment of glutathione-dependent defence system in the liver of rats repeatedly treated with carbon tetrachloride.

To study the effect of carbon tetrachloride treatment on hepatic lipid peroxidation and glutathione-dependent defence system, rats were injected with carbon tetrachloride (0.2 ml/kg body weight, i.p.

Lipid peroxidation in liver, plasma, and erythrocytes of rats chronically treated with ethanol.

The effect of ingestion of water containing 20% ethanol for 1-2 months on lipid peroxide levels of liver, plasma, and erythrocyte was investigated in rats. Our results show that elevated plasma lipid peroxide levels and erythrocyte susceptibility to lipid peroxidation may reflect stimulated lipid peroxidation in rat liver following chronic ethanol ingestion.

The effect of chronic ethanol ingestion on hepatic lipid peroxide, glutathione, glutathione peroxidase and glutathione transferase in rats.

Water containing 20% ethanol was given for a period of 3, 6 and 9 weeks to rats, and changes in hepatic lipid peroxide, glutathione, glutathione peroxidase and glutathione transferases were investigated. Lipid peroxide levels and glutathione peroxidase activities remained unchanged after 3 weeks and started to increase thereafter. Glutathione levels and glutathione transferase activities were significantly increased following ethanol consumption.

Influence of acute ethanol administration on hepatic glutathione peroxidase and glutathione transferase activities in the rat.

Acute ethanol administration to rats fasted overnight resulted in increased lipid peroxide levels and decreased glutathione content in the liver. In this condition, hepatic glutathione peroxidase activity remained unchanged, whereas glutathione transferase activity was decreased.

The in vitro enzymatic conjugation of glutathione with L-thyroxine.

Enzymatic-reaction of glutathione (GSH) with L-thyroxine formed a GSH-L-thyroxine conjugate, shown by disappearance of GSH from the incubation mixture at fixed intervals and by the use of chromatographic techniques.