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Updated: May 17, 2026

Trans-Tympanic Drug Delivery for the Treatment of Ototoxicity
Published on: March 16, 2018
Cisplatin and aminoglycoside antibiotics: hearing loss and its prevention
Jochen Schacht1, Andra E Talaska, Leonard P Rybak
1Department of Otolaryngology, Kresge Hearing Research Institute, University of Michigan, Ann Arbor, Michigan 48109-5616, USA. schacht@umich.edu
Abstract:
This review introduces the pathology of aminoglycoside antibiotic and the cisplatin chemotherapy classes of drugs, discusses oxidative stress in the inner ear as a primary trigger for cell damage, and delineates the ensuing cell death pathways. Among potentially ototoxic (damaging the inner ear) therapeutics, the platinum-based anticancer drugs and the aminoglycoside antibiotics are of critical clinical importance. Both drugs cause sensorineural hearing loss in patients, a side effect that can be reproduced in experimental animals. Hearing loss is reflected primarily in damage to outer hair cells, beginning in the basal turn of the cochlea. In addition, aminoglycosides might affect the vestibular system while cisplatin seems to have a much lower likelihood to do so. Finally, based on an understanding the mechanisms of ototoxicity pharmaceutical ways of protection of the cochlea are presented.
Insights
Aminoglycoside antibiotics and cisplatin chemotherapy cause inner ear damage, leading to hearing loss by triggering oxidative stress and cell death. Understanding these mechanisms may lead to protective pharmaceutical strategies.
Area of Science:
- Ototoxicity research
- Cellular and molecular biology
- Pharmacology
Background:
- Aminoglycoside antibiotics and cisplatin chemotherapy are clinically important drugs with ototoxic potential.
- Both drug classes can induce sensorineural hearing loss, primarily affecting cochlear outer hair cells.
- Aminoglycosides may also impact the vestibular system, whereas cisplatin has a lower likelihood of doing so.
Purpose of the Study:
- To review the pathology of aminoglycoside and cisplatin ototoxicity.
- To discuss the role of oxidative stress in inner ear cell damage.
- To delineate cell death pathways and explore pharmaceutical protection strategies.
Main Methods:
- Review of existing literature on aminoglycoside and cisplatin ototoxicity.
- Analysis of mechanisms involving oxidative stress and cell death pathways in the inner ear.
- Exploration of potential pharmaceutical interventions for cochlear protection.
Main Results:
- Oxidative stress is identified as a key trigger for ototoxicity in the inner ear.
- Specific cell death pathways are delineated following drug-induced damage.
- Outer hair cell damage in the basal cochlea is a primary manifestation of hearing loss.
Conclusions:
- Understanding the molecular mechanisms of ototoxicity is crucial for developing protective therapies.
- Pharmaceutical strategies targeting oxidative stress and cell death pathways show promise for preventing cisplatin and aminoglycoside-induced hearing loss.
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