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김우중(Woo Joong Kim),천진옥(Jin Ok Chun),홍은경(Eun Gyoung Hong),성현주(Hyun Joo Sung),임인기(In Kee Rim),전용철(Yong Cheol Jeon),전노원(Rho Won Chun),이명석(Myung Seok Lee),정규원(Kyu Won Chung) 대한내과학회 1995 대한내과학회지 Vol.48 No.1
N/A Objectives: It is well known that adult experimental rats parenterally poisoned with a lethal dose of phalloidin die of hemorrhagic necrosis of liver. Although the precise mechanism is unknown so far, it is believed that interaction of microfilamentous structures with phalloidin is the primary toxic event of phalloidin poisonings. The purpose of these experiments was to examine the influence of phalloidin on hepatocyte ultrastructure, and to determine the possible mechanism by which this agents interferes with normal microfilament function. Methods: Rats were divided into 3 groups: normal control, intravenously phalloidin injected group (10 min, 30 min and 60 min group respectively), intraperitoneally phalloidin administered group (1st day, 7th day and 14th day group respectively). At the time of sacrifice, blood was withdrawn for liver function tests and the liver tissues were observed under the light microscope and transmission electron microscope. Results: 1) Compared with control, the ratio of liver/body weight increased from 30 minutes and sustained in elevated level unti114 days after phalloidin administration. 2) Liver function test showed no significant change in serum bilirubin levels, but serum glucose levels decreased significantly in intravenously injectioned group than that of control. SGOT levels were elevated through experimental period and SGPT levels were higher in 60 minute and 14th day groups than that of control. 3) Light microscopic examination in the intravenously injected group showed highly vacuolized cytoplasm with erythrocytes-containing vacuoli in the hepatocytes and the foci of hemorrhagic necrosis scattered throughout the hepatic lobules. No significant changes in liver tissue were noted light microscopically in intraperitoneally administered group. 4) Transmission electron microscopic examination in the intravenously injected group revealed numerous variously sized vacuoles filled with erythrocytes and fibrins in the cytoplasm of hepatocyte. In intraperitoneally administered group, proliferation of microfilaments beneath the plasma membrane of hepatocytes, canalicular luminal dilation and loss of canalicular microvilli were most prominent findings. Conclusion: Hepatic injury induced by intravenous and intraperitoneal administration of phalloidin mainly involves cytoplasmic vacuole formation in the hepatocytes and proliferation of microfilaments especially around bile canaliculus, respectively. This effect of phalloidin may prove a useful tool for the study of drug-induced liver injury and of the role of microfilament in the process of bile secretion.
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