1.Phospholipidosis of Liver Induced by Amiodarone.
Dong Hoon KIM ; Gium Mi JANG ; In Soo SUH ; Tae Joong SOHN
Korean Journal of Pathology 1991;25(1):1-10
Ultrastructural study of the effects of amiodarone on the liver tissue was performed. Rats were fed with amiodarone containing diet and were sacrificerd at 1st, 3rd, 4th, 5th and 8th weeks of experiment. Charateristic lisosomal inclusion bodies were appeared form first week, which were more prominent and increased in size at the 5th and 8th week of experiment. These inclusion bodies were found in hepatocytes, Kupffer cells, bile duct epithelial cells and fibroblasts but most prominent in hepatocytes. The lysosomal inclusion bodies could be divided into four types; those characterized by (1) dense bodies with packed crystaloid contents, (2) multilamellated bodies, (3) irregular shaped bodies with varying electron density and 4. dense bodies containing stacks of fine membranous structures. All types were found in all experimental groups. But the type 1 and 2 were predominent at early stage, while type 3 and 4 were more prominent at later stage According to these findings, the formation of the lysosmal inclusion body was a characteristic change in derangement of phospholipid metabolism. And amiodarone could induce disturbance of phospholipid metabolism in all kinds of cells in liver tissue.
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2.The Effect of Common Bile Duct Ligation on Liver Morphology and Coper Metabolism in Rat.
Kyoung Sook KIM ; Chanil PARK ; Jang Whan CHO ; In Joon CHOI ; Yoo Bock LEE
Korean Journal of Pathology 1990;24(4):402-411
To clarity the effect of biliary obliteration on copper metabolism of rat liver and on the hepatic morphology, 0.5% cuppuric sulfate was administered intraperitoneally for 42 days following ligation of the common bile duct (CBD) of Sprague-Dawley rats. The blood copper concentration, the hepatic copper content and the accumulation patterns of copper and copper binding protein in the liver were examined and compared with those of the simple CBD ligation group and the simple copper over loaded group. CBD ligation induced marked proliferation of bile ductular structures which, after expanding the portal tracts, invaded and divided the hepatic lobules. There was, however, no excess fibosis beyond what needed to support the new ductules. The blood copper concentration and the hepatic copper content were increased by copper overload with or without CBD ligation, particularly incases with CBD ligation. Liver cell necrosis did not occur by the overloaded copper alone in rats. The hepatic copper and copper binding protein were accumulated at periportal liver cells in the group of coppe overload after CBD ligatio, whereas they began to appear at perivenular hepatocytes in the simple copper overloaded group. In conclusion, it is suggested that CBD ligation does not induce excess fibrosis or liver cirrhosis in rat as far as during our experimental period, but affect significantly on copper metabolism by intrahepatic redistribution of the copper and the copper binding proteins.
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3.Ultrastructural Studies of Aortic Endothelial Injury and Regeneration.
Gium Mi JANG ; Dong Hoon KIM ; Jyung Sik KWAK ; Tae Joong SOHN
Korean Journal of Pathology 1990;24(4):337-348
Author performed this experiment to define the most important factor preventing the intimal thickening. An endothelium of abdominal aorta in the rat was denuded by two different wires having same caliver. The degree of injury was limited to the endothelial cells in one, and extended to the internal elastic lamina in another. The results showed that at 72 hours, in the case of superficial injury, the entire injury site was covered by new regenerating cells, but in the case of disruption of the internal elastic lamina, the migrating smooth muscle cell completely reached into the intima and resulted in intemal thickening. Similar findings persisted to 1 week later. Above results suggest the most important factor preventing the intimal thickening in endothelial injury is the depth of the injury which limited within the endothelial cells without extending into the internal elastic lamina and medial smooth muscle cells.
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4.Ultrastructural Changes of Lead Acetate Induced Liver Injury in Rats.
Korean Journal of Pathology 1996;30(3):184-198
To evaluate the ultrastructural changes and the mechanism causing liver injury by lead, light and electron microscopic(LM and EM) examination using Timm sulphide silver method(TSM) was done. Sprague-Dawley rats were divided into a control and 3 experimental groups. The experimental groups were orally administered 0.5% lead acetate(LA). Group 1 received a one time dose of 10 ml of LA by gastric intubation. Groups 2 and 3 continuously received LA instead of drinking water. The control group was composed of 3 rats in each group which did not receive any treatment. Rats of group 1, 2 and 3 and control were sacrificed at 1/2, 1, 1 1/2 hours, 2 days, and at 1, 2, 4, 6 and 8 weeks later, except group 3. Before sacrifice, they were perfused with 0.1% sodium sulphide and 2.5% glutaraldehyde through the abdominal aorta for TSM. The liver was taken for LM and EM examinations. Blood lead concentration began to increase from the 2nd day up to 3.29 microgram/ml at 2nd week, and the urinary delta-ALA level showed a steady increase from the 2nd day. LM and EM examination of liver revealed that absorbed lead granules in group 1 were transported into sinusoidal spaces, Kupffer cells, and the hepatocytes within 1 hour and then disappeared 1/2 hour thereafter. In group 2 deposited lead was found in the hepatocytic cytosol bound to mitochondria. That in turn inhibited mitochondrial respiration with resultant mitochondrial swelling at the 1st week and thereafter at 6th week myelin figure formation and condensation of mitochondria, and peroxisomes were increased at 8th week. Based on these results it can be concluded that a transient intake of subletal dose of LA is biotransformed completely by periportal hepatocytes within 1 1/2 hours, but excessively accumulated lead can induce liver cell injury due to lipid peroxidation of membrane by direct toxic effect of lead and by products of lipid peroxidation. We postulate that lead acetate triggers presumably primarily mitochondrial membrane injury and then other organellar changes may play a role in disturbance of a network of interacting of key events capable of causing cell death.
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5.Ultrastructural Changes of the Bile Canaliculi after Common Bile Duct Ligation.
Kook Seon YOO ; Suk Hee LEE ; Hee Kyung PARK ; Chang Ho CHO ; Jong Min CHAE
Korean Journal of Pathology 1996;30(3):175-183
The purpose of this study was to investigate the morphologic changes of the bile canaliculi and its associated structures of the liver induced by common bile duct ligation(CBDL) in the rat. The canalicular surface and lateral surface of the dry-fractured hepatocytes was studied with scanning electron microscopy at 1~6 weeks post ligation. The first week after CBDL, the bile canaliculi were dilated. The microvilli were increased in number and the lumens contained granular materials After 2 weeks or more, the bile canaliculi were dilated to a variable degree, and with irregularity, measuring from 1.5 to 5 micrometer in diameter, and in the advanced stage, the canaliculi showed blunting and the disappearance of microvilli. Some canaliculi had sprouting side branches. At 4~6 weeks post-ligation, the lateral surface of the hepatocytes also showed some irregularity and a tortuous appearance, and numerous small sized microvillous projections were formed. The tubular structures of the proliferated SER distributed adjacent to the lateral surface of the hepatocytes, and the direct connection of a tubular structure and the cytoplasmic membrane was observed. These results suggest that the deformity and loss of microvilli of bile canaliculi reflect the disturbance of bile secretion from the hepatocytes. And prolonged obstruction of bile flow may result in bile excretion via the lateral surface of hepatocytes.
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9.An Ultrastructural Study on the Small Intestinal Absorptive Cells of Rat after Administration of Lead Acetate.
Dong Sug KIM ; Kee Kwon KIM ; Eun Sook CHANG
Korean Journal of Pathology 1994;28(6):559-568
This study was carried out to visualize lead by Timm sulphide silver method and to define lead-induced change of duodenal absorptive cells of rat after administration of 0.01% lead acetate with drinking water. Sprague-Dawley rats, weighing 250g, were used, and they were orally administered with 0.01% sodium acetate and sacrificed at 0.5, 1, 1.5 hours and 2, 7, 15, 30, 45, 60 days after administration. A portion of duodenal tissue was observed under light microscope, scanning and transmission electron microscopes after development with Danscher method. The blood lead concentration in experimental group began to increase from the 2nd day after administration, and it increased gradually until the 45th day and decreased at the 60th day. On light microscope, many brown lead granules were observed at the villi tip at the 2nd day. There is mild blunting of villi tip at the 45th day. At the 60th day, most of the villi were mildly shortened and showed lymphangiectasia. On scanning electron microscope, the villi tip was mildly blunted and the extrusion zone became irregular at the 45th day. The depth of creases did not change. At the 60th day, the villi tip was moderately blunted and the extrusion zone was markedly irregular. The depth of creases increased. On transmission electron microscope, at 0.5 hour after oral administration, numerous lead granules were diffusely scattered and were not confined to any specific microorganelles. The lead granules decreased with time. At the 7th 15th day, the intercellular spaces were widened and several vacuoles appeared and the condensation of mitochondrial matrix. There was also ribosomal detachment from RER, and there was neither secondary lysosomes or post-lysosomes. At the 30th and 45th day, secondary lysosomes appeared and the condensation of mitochondrial matrix with early formation of myelin figures was noted. At the 60th day, the intercellular space widening extended to the upper most portion of the cells, and nonspeciqic degenerative changes became severe. In view of above mentioned findings, it can be concluded that passive diffusion as well as active transport was partly involved in the absorption of lead. Most of the changes of microorganelle are compatible with nonspecific degenerative changes which could occur due to impairment of oxidative phosphorylation.
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