Lipopolysaccharide-induced cytotoxicity against cultured mouse hepatocytes and the role of nonparenchymal liver cells.
Lipopolysaccharide (LPS) was found to induce significant hepatocytotoxicity against cultured mouse hepatocytes. Degeneration and necrosis of cultured hepatocytes and decrease of hepatocyte viability were prominent. The aspartate transferase level and 3H-TdR release in the medium were significantly increased after treatment, and the degree of these changes paralleled with LPS concentration. Various other parameters showed no significant difference between the hepatocytes cultured alone and those cocultured with nonparenchymal liver cells. However, if the nonparenchymal liver cells were isolated from mice which had been pretreated with D-galactosamine (GalN) not only was the hepatocytotoxicity induced by LPS enhanced, but the cells also showed certain cytotoxicity against cultured hepatocytes even without LPS. These results suggest that nonparenchymal liver cells might promote LPS-induced hepatocyte injury.
Wang
Y
Y
Department of Infectious Diseases, Southwest Hospital, Third Military Medical College, Chongqing.
Hiroo
O
O
Yasutoshi
M
M
Liu
P
P
D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002478:Cells, Cultured; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008099:Liver / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D013936:Thymidine / Q000378:metabolism
D008070:Lipopolysaccharides; D001219:Aspartate Aminotransferases; D013936:Thymidine