ABSTRACT
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.). Furthermore, it has been determined that cytosolic glutathione S-transferase (GST) activity was decreased and glutathione peroxidase (GSH-Px) activity remained unchanged. On the other hand, a decrease in liver microsomal lipid peroxide levels and an increase in GST and GSH-Px activity has been observed. We concluded that decreased lipid peroxide levels in microsomes could be a consequence of increased GSH-Px and GST enzyme activities. In this way, these glutathione-related defence enzyme systems may play an important role in protecting microsomes from lipid peroxidation.
Subject(s)
Acetaminophen/toxicity , Glutathione/metabolism , Lipid Peroxidation/drug effects , Liver/drug effects , Liver/enzymology , Animals , Cytosol/drug effects , Cytosol/enzymology , Glutathione Peroxidase/metabolism , Glutathione Transferase/metabolism , In Vitro Techniques , Male , Mice , Mice, Inbred BALB C , Microsomes, Liver/drug effects , Microsomes, Liver/enzymology , Oxidative Stress/drug effects , Oxidative Stress/physiologyABSTRACT
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.
Subject(s)
Cholestasis, Intrahepatic/metabolism , Copper/metabolism , Lipid Peroxidation/physiology , Liver Cirrhosis, Experimental/etiology , Liver/metabolism , Alanine Transaminase/metabolism , Alkaline Phosphatase/metabolism , Animals , Aspartate Aminotransferases/metabolism , Bile Acids and Salts/metabolism , Bilirubin/metabolism , Cholestasis, Intrahepatic/complications , Cholestasis, Intrahepatic/pathology , Diet , Disease Models, Animal , Hydroxyproline/metabolism , Liver Cirrhosis, Experimental/metabolism , Male , Rats , Rats, Inbred StrainsABSTRACT
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.) led to an increase in lipid peroxide levels and a decrease in glutathione levels in whole brain homogenates without cerebellum. However, there was no change in brain lipid peroxide and glutathione levels of rats chronically treated with ethanol.
Subject(s)
Brain/drug effects , Ethanol/toxicity , Glutathione/metabolism , Lipid Peroxidation/drug effects , Alcoholic Intoxication/pathology , Alcoholism/pathology , Animals , Brain/pathology , Liver/pathology , Male , Malondialdehyde/metabolism , Rats , Rats, Inbred StrainsABSTRACT
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.
Subject(s)
Cholestasis/metabolism , Lipid Peroxidation , Microsomes, Liver/metabolism , NADP/metabolism , Animals , Bile Acids and Salts/analysis , Bilirubin/analysis , Cholestasis/enzymology , Cholesterol/metabolism , Cytochrome P-450 Enzyme System/metabolism , Male , Phospholipids/metabolism , Rats , Rats, Inbred StrainsABSTRACT
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.
Subject(s)
Brain/metabolism , Ethanol/pharmacology , Glutathione/metabolism , Lipid Peroxides/metabolism , Liver/metabolism , Animals , Male , Rats , Rats, Inbred StrainsABSTRACT
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.) twice weekly for a period of 4 weeks. Carbon tetrachloride treatment caused a significant increase in hepatic lipid peroxide levels and significant decreases in hepatic glutathione levels and glutathione peroxidase and glutathione transferase activities. These results show that chronic carbon tetrachloride administration to rats leads to the stimulation of hepatic lipid peroxidation, which seems to be the consequence of impaired cellular defence by glutathione and glutathione-related enzymes.
Subject(s)
Carbon Tetrachloride Poisoning/metabolism , Glutathione/physiology , Lipid Peroxides/metabolism , Liver/drug effects , Animals , Body Weight/drug effects , Carbon Tetrachloride Poisoning/enzymology , Glutathione Peroxidase/metabolism , Glutathione Transferase/metabolism , Liver/enzymology , Liver/metabolism , Male , Organ Size/drug effects , Rats , Rats, Inbred Strains , Time Factors , Triglycerides/metabolismABSTRACT
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.
Subject(s)
Erythrocytes/metabolism , Ethanol/toxicity , Lipid Peroxides/metabolism , Liver/metabolism , Plasma/metabolism , Animals , Lipid Peroxides/blood , Male , Rats , Rats, Inbred Strains , Time FactorsABSTRACT
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. These results show that chronic ethanol consumption stimulates hepatic lipid peroxidation in rats. This stimulation is not dependent on glutathione depletion and the increased glutathione peroxidase and glutathione transferase activities may reflect an adaptive change against ethanol-induced lipid peroxide toxicity.
Subject(s)
Alcoholism/metabolism , Glutathione/metabolism , Lipid Peroxides/metabolism , Liver/metabolism , Alcoholism/enzymology , Animals , Glutathione Peroxidase/metabolism , Glutathione Transferase/metabolism , Humans , Liver/drug effects , Liver/enzymology , Male , Rats , Rats, Inbred Strains , Time FactorsABSTRACT
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.
Subject(s)
Ethanol/pharmacology , Glutathione Peroxidase/metabolism , Glutathione Transferase/metabolism , Liver/enzymology , Alanine Transaminase/blood , Animals , Aspartate Aminotransferases/blood , Lipid Peroxides/metabolism , Male , Rats , Rats, Inbred StrainsABSTRACT
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.
