Journal Article

Insights into potential cellular mechanisms of cisplatin nephrotoxicity and their clinical application.

M K Kuhlmann, G Burkhardt and H Köhler

in Nephrology Dialysis Transplantation

Volume 12, issue 12, pages 2478-2480
Published in print December 1997 | ISSN: 0931-0509
Published online December 1997 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/12.12.2478
Insights into potential cellular mechanisms of cisplatin nephrotoxicity and their clinical application.

Show Summary Details

Preview

Cisplatin preferentially accumulates in cells of the S3 segment of the renal proximal tubule and is toxified intracellularly by hydration. The earliest manifestation of toxicity is inhibition of protein synthesis. GSH depletion is another important mechanism causing CP toxicity. Intracellular binding to SH groups leads to GSH depletion, resulting in lipid peroxidation and eventually mitochondrial damage. New measures to prevent GSH depletion and scavenge intracellular free oxygen radicals have been tried in clinical studies. Promising results indicate that cisplatin nephrotoxicity can be further reduced in the future.

Journal Article.  0 words. 

Subjects: Nephrology

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.