Journal of Pathology and Translational Medicine

Original Articles

Ultrastructural Feature of Proximal Convoluted Tubular Cells of Rat Induced by Gentamicin.: Byoung Yuk Lee, Tae Jung Shon, Jong Min Chae; Korean J Pathol. 1998;32(1):43-50.

Abstract PDF: Myeloid body formation is an ultrastructural feature of gentamicin induced nephrotoxicity in human being and experimental animals. The origin of the myeloid body is not satisfactorily understood and morphological verification of the developing process of this structure is not fully accomplished. We injected 100 mg/kg/12 hour of gentamicin in 20 Spraque-Dawley rats and examined the ultrastructural feature of the proximal convoluted tubular cells of the kidney every 30 minutes in the first 4 hours, and in 5 hours, 6 hours, 12 hours, 24 hours and 48 hours after injection of gentamicin, with a TEM and a SEM. Myeloid bodies were noted as concentric layers of membranous structures of degenerated endoplasmic reticulum and mitochondria in the lysosome. The number and size of the myeloid body containing lysosomes were increased with time. We can deduce from this observation that injured cell organelles by diffusible gentamicin within the cells are autophagocytosed by lysosomes which were also injured by the drug from pinocytotic vesicles, and incompletely digested organellar remnants are retained in the lysosomes as myeloid bodies. So we think that the myeloid body formation is a result of an exaggerated and a pathologic autophagocytic process due to cell injury induced by gentamicin.

Cyclosporine Toxicity on Cultured Human Renal Proximal Tubular Cells.: Jung Young Lee; Korean J Pathol. 1990;24(4):423-429.

Abstract PDF: Nephrotoxicity is the most common dose-limiting factor of cyclosporine A (CSA) in clinical usage. But the mechanism of CSA-induced nephrotoxicity still remains unresolved. Many authors insisted that CSA induced renal proximal tubular cell injury is due to the secondary effects following hemodynamic changes or endothelial cell damage, instead of direct toxicity by CSA. To find out that CSA has a direct toxicity to the proximal tubular cells, the author used primary cultures of human proximal tubular cells to eliminate the hemodynamic or endothelial influences that could be produced in in vivo model. In the present study, the viability against CSA was tested by the neutral red assay method with modulation of Ca2+ amount in incubating media and observed electron microscopically. The viability test showed direct toxic effect of CSA on human proximal tubular cells and this was enhanced by Ca2+ depletion in incubating media. Morphologically noted are accumulation of lipid droplets and polyribosomal dispersion, which may be association with inhibition of cellular synthetic activity. These results suggest the toxixity is a direct effect of cyclosporine and that toxic mechanism may be due to inhibition of cellular synthetic activity. And this experiment also showed that primary cultures of human renal proximal tubular cells can be a good in in vivo model for investigating CSA nephrotoxicity.

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