Modification of galactosamine-induced liver injury in rats by reticuloendothelial system stimulation or depression

Authors

  • Ali Al-Tuwaijri,

    1. Departments of Physiology and Medicine, Tulane University School of Medicine, New Orleans, Louisiana 70112
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  • Kemal Akdamar,

    1. Departments of Physiology and Medicine, Tulane University School of Medicine, New Orleans, Louisiana 70112
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  • Nicholas R. di Luzio Ph.D.

    Professor and Chairman, Corresponding author
    1. Departments of Physiology and Medicine, Tulane University School of Medicine, New Orleans, Louisiana 70112
    • Department of Physiology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, Louisiana 70112
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Abstract

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.

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