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Updated: Jul 26, 2025
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Trans-Tympanic Drug Delivery for the Treatment of Ototoxicity
Published on: March 16, 2018
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Protective Effects of Infliximab Against Kanamycin-Induced Ototoxicity in Rats
Pelin Koçdor, Esra Özkan1, Fatmanur Akpunar1
1Koç University Research Center for Translational Medicine, Istanbul.
Summary
Infliximab (INF) protected against kanamycin (KM)-induced hearing loss in rats, particularly at lower doses. Tumor necrosis factor-based inflammation is implicated in KM ototoxicity.
Area of Science:
- Ototoxicity research
- Pharmacology of hearing loss
- Inflammation and cellular damage
Background:
- Tumor necrosis factor-alpha (TNF-α) blockers can mitigate inflammatory responses and cell death.
- Understanding the role of inflammation in drug-induced hearing loss is crucial.
Purpose of the Study:
- To investigate the protective efficacy of infliximab (INF) against kanamycin (KM)-induced ototoxicity.
- To explore the role of TNF-α in kanamycin-induced hearing damage.
Main Methods:
- Rats were divided into groups receiving varying doses of KM, INF, or methylprednisolone (MP).
- Auditory brain-stem response (ABR) was used to assess hearing thresholds.
- Cochlear tissues were analyzed for stria vascularis area, spiral ganglion neurons, hair cell fluorescence, postsynaptic densities (PSD), and presynaptic ribbons (PSRs).
Main Results:
- Kanamycin significantly increased hearing thresholds by day 14.
- Infliximab preserved hearing and cochlear structures (hair cells, PSDs, PSRs) when administered with low-dose KM.
- Methylprednisolone treatment resulted in significantly lower hair cell fluorescence and synaptic structures compared to controls.
Conclusions:
- Tumor necrosis factor-driven inflammation appears to be a key factor in the mechanism of kanamycin-induced ototoxicity.
- Infliximab shows potential as a protective agent against certain types of drug-induced hearing loss.
