dolichol-monophosphate-mannose has been researched along with Chemical-and-Drug-Induced-Liver-Injury* in 2 studies
2 other study(ies) available for dolichol-monophosphate-mannose and Chemical-and-Drug-Induced-Liver-Injury
| Article | Year |
|---|---|
Inflammation-induced increases in dolichol synthesis and hydroxymethylglutaryl-coenzyme A reductase activity in mouse liver are prevented by a high-cholesterol diet but not by fasting.
The inflammatory response in mammals is characterized by the synthesis in the liver of several N-linked serum glycoproteins called acute-phase reactants. In C57BL/6J mice, turpentine-induced inflammation was accompanied by increases in 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity, dolichol synthesis, and dolichyl phosphoryl mannose synthesis. Cholesterol feeding, but not fasting, prevented these inflammation-induced increases in reductase activity and dolichol synthesis. However, the rate of incorporation of [3H]mannose into total serum glycoproteins was not affected by the high-cholesterol diet, and this rate increased during acute inflammation in control and cholesterol-fed mice. Topics: Acetates; Acetic Acid; Animals; Chemical and Drug Induced Liver Injury; Cholesterol, Dietary; Diterpenes; Dolichol Monophosphate Mannose; Dolichols; Fasting; Hydroxymethylglutaryl CoA Reductases; In Vitro Techniques; Liver; Male; Mice; Mice, Inbred C57BL; Microsomes, Liver; Tritium | 1984 |
Effect of dexamethasone on mannolipid synthesis by hepatocytes prepared from control and inflamed rats.
Hepatocytes were prepared from control and inflamed rats. Mannose incorporation into dolichol monophosphate mannose in homogenate and microsomal fraction of the hepatocytes was increased 2-fold over the controls 24 h after induction of inflammation by turpentine injection. Incubation of hepatocytes from both control and inflamed rats with 0.1-10 microM-dexamethasone produced a 1.5-fold increase of dolichol phosphate mannose formation, whereas, 100 microM-dexamethasone decreased its formation. The increase in the ratio of dolichol phosphate mannose formation in inflamed over controls was virtually eliminated when the cell homogenate assay mixtures included 30 nmol of exogenous dolichol phosphate. This supports the earlier suggestion that the increase in the enzyme activity in inflammation could be due to higher concentrations of endogenous dolichol phosphate [ Coolbear & Mookerjea (1981) J. Biol. Chem. 256, 4529-4535]. In contrast, the increase in the ratio of dolichol phosphate mannose formation between dexamethasone-treated and untreated hepatocytes remained unchanged when increasing concentrations of exogenous dolichol phosphate were added to the assays. This suggests that the increase in glycosylation of dolichol phosphate in dexamethasone-treated hepatocytes is probably due to the increased mannosyltransferase activity, rather than due to higher concentrations of endogenous dolichol phosphate in these cells. Topics: Animals; Chemical and Drug Induced Liver Injury; Culture Media; Dexamethasone; Dolichol Monophosphate Mannose; Dose-Response Relationship, Drug; In Vitro Techniques; Liver; Male; Mannosyltransferases; Polyisoprenyl Phosphate Sugars; Rats; Rats, Inbred Strains; Subcellular Fractions | 1984 |