Studies into the mechanism of reversal of experimental acute hepatic failure by hepatocyte transplantation. 1.
The authors reported previously that single cell suspensions of syngeneic, allogeneic and xenogeneic hepatocytes can significantly improve survival in a rat model of acute hepatic failure induced by D-galactosamine. This report explores the mechanism by which hepatocyte transplantation reverses the toxin-induced hepatic necrosis. Radioautographic studies indicated that intraperitoneally administered hepatocytes labelled with tritiated thymidine did not repopulate the injured recipient liver. Hepatocytes irradiated with 10 000 rad (i.e., the cells were nonreplicating) also resulted in a significant (P less than 0.001) increase in animal survival when given to rats treated with D-galactosamine. Experiments with subcellular fractions of hepatocytes demonstrated that an intact cell was not required and that a heat stable "factor" (or factors) present in the cytosol fraction, which is not insulin or glucagon, is responsible for the increase in survival observed. This factor appears to increase the rate of endogenous regeneration of the injured recipient liver.
D000818:Animals; D056486:Chemical and Drug Induced Liver Injury; D003600:Cytosol / Q000378:metabolism; D005260:Female; D005688:Galactosamine; D006082:Graft Enhancement, Immunologic; D008099:Liver / Q000166:cytology; D008107:Liver Diseases / Q000628:therapy*; D008115:Liver Regeneration; D016031:Liver Transplantation; D008297:Male; D011817:Rabbits; D051381:Rats; D013552:Swine; D013936:Thymidine / Q000378:metabolism; D014183:Transplantation, Heterologous; D014184:Transplantation, Homologous; D014316:Tritium
D014316:Tritium; D005688:Galactosamine; D013936:Thymidine