Induction of prothrombin biosynthesis and inhibition of gamma carboxylase activity in experimental models of liver regeneration and fibrosis.
1. When acute liver damage is induced in rats treated with CCl4, both prothrombin biosynthesis and gamma carboxylase activity decreases, originating a prolongation of prothrombin time in plasma. 2. Then, during the regenerative process, prothrombin biosynthesis increases higher than normal, but gamma carboxylase activity remain decreased. In this case, prolongation of prothrombin time occurs in spite of high levels of descarboxylated prothrombin in plasma. 3. An increase of descarboxylated prothrombin in plasma is also detected in the CCl4-liver fibrosis model.
Panduro
A
A
Department of Gastroenterology, Instituto Nacional de la Nutrición S.Z., Tlalpan, México, D.F.
Valencia
J
J
Rojkind
M
M
D000818:Animals; D002251:Carbon Tetrachloride; D019735:Carbon-Carbon Ligases; D008025:Ligases / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000378:metabolism*; D008115:Liver Regeneration / Q000502:physiology*; D008297:Male; D014176:Protein Biosynthesis; D011499:Protein Processing, Post-Translational; D011516:Prothrombin / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D014757:Viper Venoms / Q000494:pharmacology
D014757:Viper Venoms; D011516:Prothrombin; D002251:Carbon Tetrachloride; D008025:Ligases; D019735:Carbon-Carbon Ligases; C020660:glutamyl carboxylase