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Effect of Cisplatin on Sodium-Dependent Hexose Transport in LLC-$PK_1$ Renal Epithelial Cells

Lee, Suk-Kyu   (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College  ); Kim, Jee-Yeun   (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College  ); Yu, Tai-Hyun   (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College  ); Kim, Kyoung-Ryong   (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College  ); Kim, Kwang-Hyuk   (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College  ); Park, Yang-Saeng   (Departments of Otolaryngology, Physiology, and Microbiology Kosin Medical College  );
  • 초록

    Cis-dichlorodiammine platin ${\mu}M$ II (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- $PK_1$ 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 ${\alpha}-methyl-D-[^{14}C]glucopyranoside$ (AMG) as a model substrate. In cells treated with 100 ${\mu}M$ cisplatin, the AMG uptake was progressively impaired after 3 days. The viability of cells was not substantially changed with cisplatin of less than 100 ${\mu}M$ , but it decreased markedly with 150 and 200 ${\mu}M$ . 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- $PK_1$ 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.


  • 주제어

    cisplatin .   $LLC-PK_1$ cell .   Na-hexose cotransport .   phlorizin.  

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