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Toxicol Lett. 2015 Sep 17;237(3):219-27. doi: 10.1016/j.toxlet.2015.06.012. Epub 2015 Jun 20.

An integrated view of cisplatin-induced nephrotoxicity and ototoxicity.

Author information

1
Oregon Hearing Research Center, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, United States.
2
Oregon Hearing Research Center, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, United States. Electronic address: steygerp@ohsu.edu.

Abstract

Cisplatin is one of the most widely-used drugs to treat cancers. However, its nephrotoxic and ototoxic side-effects remain major clinical limitations. Recent studies have improved our understanding of the molecular mechanisms of cisplatin-induced nephrotoxicity and ototoxicity. While cisplatin binding to DNA is the major cytotoxic mechanism in proliferating (cancer) cells, nephrotoxicity and ototoxicity appear to result from toxic levels of reactive oxygen species and protein dysregulation within various cellular compartments. In this review, we discuss molecular mechanisms of cisplatin-induced nephrotoxicity and ototoxicity. We also discuss potential clinical strategies to prevent nephrotoxicity and ototoxicity and their current limitations.

KEYWORDS:

Cisplatin; Intracellular mechanisms; Nephrotoxicity; Ototoxicity

PMID:
26101797
PMCID:
PMC4516600
DOI:
10.1016/j.toxlet.2015.06.012
[Indexed for MEDLINE]
Free PMC Article

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