Abstract
Abstract
D-Galactosamine is an amino sugar with unique hepatotoxic properties in animals. Although the mechanism of liver injury by galactosamine remains controversial, a role for bacterial endotoxin has been suggested. In the present study, using New Zealand rabbits, we show that the significant increase in serum glutamic oxaloacetic transaminase which followed the injection of 4.25 mmole/kg of D-galactosamine was completely prevented in animals subjected to resection of small bowel and colon. Using an immunoradiometric assay specific for E. coli 026 endotoxin we showed that after instillation of 50 mg of E. coli into the colon, serum levels of this endotoxin were higher in the animals injected with galactosamine than the controls injected with saline. However, the differences in endotoxin concentration between the two groups of animals was statistically significant only at 30 and 60 min. The role of endotoxin in the pathogenesis of galactosamine liver injury is reviewed and discussed.
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