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- Ultrastructural Changes in Rat Kidney after Lead Acetate Administration.
- Hyun Chul Kim, Seung Pil Kim, Kwan Kyu Park
- Korean J Pathol. 1996;30(2):73-88.
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Abstract
PDF - This study was carried out to investigate the ultrastructural findings of rats after administration of 0.5% lead acetate with drinking water. The Sprague-Dawley rats were divided into control and experimental groups. The control group was composed of 12 rats and was orally administered with 0.5% sodium acetate. The experimental group was composed of 36 rats and orally administered with 0.5% lead acetate. Two rats in the control group and four rats in the experimental group were sacrificed on day 2, and week 1, 2, 4, 6 and 8 after administration. The kidney was extirpated and examined by electron microscopy. The results obtained were as follows: The blood lead concentration in the experimental group began to increase from the second day after administration and it increased gradually until the 6th week and it decreased at the 8 week. The urinary excretion of delta-ALA also increased from the secondary and gradually increased up to the 8th week. On electron microscopic examination, the proximal tubular cells showed fat droplets, dilatation of the endoplasmic reticulum, mitochondrial swelling, increased numbers of secondary lysosomes and myelin figure-like residual bodies and intranuclear inclusion bodies. All these findings peaked at the eighth week after administration. Ultrastructural findings after Timm sulphide silver reaction revealed the lead granules in the proximal tubular lumen and between the microvilli of the proximal tubular cells without membrane-bounded. It can be concluded that most of the changes of micro-organelles are compatible with degenerative changes of lead exposure and passive diffusion of lead granules are involved in the proximal tubular cells.
- Ultrastructural Changes of Lead Acetate Induced Liver Injury in Rats.
- Eun Sook Chang, Jin Seok Oh
- Korean J Pathol. 1996;30(3):184-198.
- 1,871 View
- 36 Download
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Abstract
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- 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.
- 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 J Pathol. 1994;28(6):559-568.
- 1,726 View
- 12 Download
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Abstract
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- 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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