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

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

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 bindin...

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Bibliographic Details
Published in:Nephrology, dialysis, transplantation Vol. 12; no. 12; pp. 2478 - 2480
Main Authors: Kuhlmann, M K, Burkhardt, G, Köhler, H
Format: Journal Article
Language:English
Published: England 01-12-1997
Subjects:
Antineoplastic Agents - poisoning
Cisplatin - poisoning
Humans
Kidney - drug effects
Online Access:Get full text
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Summary: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.
ISSN:0931-0509
1460-2385
DOI:10.1093/ndt/12.12.2478