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Modification of galactosamine‐induced liver injury in rats by reticuloendothelial system stimulation or depression
Author(s) -
AlTuwaijri Ali,
Akdamar Kemal,
di Luzio Nicholas R.
Publication year - 1981
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840010204
Subject(s) - mononuclear phagocyte system , galactosamine , medicine , transaminase , bilirubin , endocrinology , chemistry , liver injury , centrilobular necrosis , biochemistry , immunology , enzyme , glucosamine
The reticuloendothelial system has been implicated in galactosamine‐induced liver injury because of a correlation between phagocytic alterations induced by colloidal carbon or endotoxin, and development of liver necrosis. To evaluate this concept, the influence of galactosamine on liver function and histology was determined in rats in which the reticuloendothelial system was normal, stimulated, or depressed. Methyl palmitate was used as a reticuloendothelial system suppressant, and glucan was used as a reticuloendothelial system activating agent. Administration of galactosamine to control rats resulted in hypoglycemia and increased serum bilirubin concentration, elevated serum glutamic oxalacetic transaminase, lactic dehydrogenase and glutamic pyruvic transaminase activities, and retention of sodium sulfobromophthalein. Histological studies revealed hepatic necrosis, and a polymorphonuclear and lymphocytic cellular infiltrate in galactosamine‐treated rats. Pretreatment of rats with methyl palmitate inhibited galactosamine‐induced alterations in serum glucose concentration, glutamic oxalacetic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammatory reactions were also reduced in methyl palmitate‐treated galactosamine‐injected animals. In contrast, activation of the reticuloendothelial system by glucan increased galactosamine‐induced alterations in serum bilirubin, glucose and cholesterol concentrations, glutamic oxalacetic transaminase, glutamic pyruvic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammation were also increased. These findings suggest that the degree of galactosamine‐induced liver injury is directly correlated with macrophage function when specific macrophage‐modifying agents are used.