D-galactosamine-induced liver injury in immunosuppressed mice.
Thymectomized DBA/2 mice, irradiated with 720 rad/min and reconstituted with syngeneic bone marrow, were treated i.p. with 1 g/kg body weight D-galactosamine-HCl (DGA). Light and electron microscopic changes characteristic of the toxic effect of the agent, such as hepatocellular cytoplasmic inclusions and unicellular necrosis, could be observed but no inflammatory reaction was detectable in the liver. The phagocytic activity of Kupffer cells proved to be unchanged in immunosuppressed animals. Liver regeneration following DGA injury took place in 120 hours exactly as in animals having an intact immune system. The experiments suggested that T-lymphocytes participate in the development of DGA-hepatitis and their absence does not influence the restoration of liver injury. The experimental system described seems to be suitable for separating primary and secondary events and also for studying the role of the immune system in toxic liver injury.
D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000276:immunology / Q000473:pathology*; D005688:Galactosamine / Q000633:toxicity*; D007165:Immunosuppression Therapy; D002479:Inclusion Bodies / Q000648:ultrastructure; D007958:Leukocyte Count; D008099:Liver / Q000473:pathology; D008115:Liver Regeneration / Q000187:drug effects; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D008854:Microscopy, Electron; D009336:Necrosis; D013934:Thymectomy; D014916:Whole-Body Irradiation
D005688:Galactosamine