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KMID : 0811719970010010035
Korean Journal of Physiology & Pharmacology
1997 Volume.1 No. 1 p.35 ~ p.43
Effect of Cisplatin on Sodium-Dependent Hexose Transport in LLC-PK1 Renal Epithelial Cells
Suk Kyu Lee
Jee Yeun Kim/Tai Hyun Yu/Kyoung Ryong Kim/Kwang Hyuk Kim/Yang Saeng Park
Abstract
Cis-dichlorodiammine platin¥ìMII (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC-PK1 cell line was selected as a cell model and the sugar transport activity was evaluated during a course of cisplatin treatment. Cells grown to confluence were treated with cisplatin for 60 min, washed, and then incubated for up to 5 days. At appropriate intervals, cells were tested for sugar transport activity using ¥á?methyl?D?[14C]glucopyranoside (AMG) as a model substrate. In cells treated with 100 ¥ìM cisplatin, the AMG uptake was progressively impaired after 3 days. The viability of cells was not substantially changed with cisplatin of less than 100 ¥ìM, but it decreased markedly with 150 and 200 ¥ìM. In cisplatin-treated cells, the Na+ -dependent AMG uptake was drastically inhibited with no change in the Na+ -independent uptake. Kinetic analysis indicated that Vmax was suppressed, but Km was not altered. The Na+ -dependent phlorizin binding was also decreased in cisplatin-treated cells. However, the AMG efflux from preloaded cells was not apparently retarded by cisplatin treatment. These data indicate that the cisplatin treatment impairs Na+ -hexose cotransporters in LLC-PK1 cells and suggest strongly that defects in transporter function at the luminal plasma membrane of the proximal tubular cells constitute an important pathogenic mechanism of cisplatin nephrotoxicity.
KEYWORD
Cisplatin, LLC-PK1 cell, Na-hexose cotransport, Phlorizin,
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