Abstract
The purpose of this study was to examine the role of endotoxin in the onset of experimental liver injury induced by carbon tetrachloride (CCl4) in rats. The reticuloendothelial function was altered by Zymosan or Lead acetate (LA), and endotoxin tolerance (ET) was induced prior to administration of CCl4. Then, the Limulus test, examinations of the reticuloendothelial function, and biochemical and histological investigations were performed using untreated rats as control. As a result, the reticuloendothelial function was found to improve significantly in Zymosan-treated rats and ET rats, while it was significantly suppressed in LA-treated rats. In untreated rats, the Limulus test was positive in many instances and the reticuloendothelial function was markedly suppressed. There was also biochemical and histological evidence of marked liver injury. Such liver injury was less severe in Zymosantreated rats and ET rats, and more severe in LA-treated rats. Such findings suggest that the severity of liver injury is related to the facility with which endotoxin produced in the intestine by CCl4 is disposed of by the reticuloendothelial system. Thus, endotoxin appeared to be involved in the onset of liver injury by CCl4.
