Ototoxic interaction of kanamycin and 3-nitropropionic acid

Chia Der Lin, Takeshi Oshima, Kiyoshi Oda, Daisuke Yamauchi, Ming Hsui Tsai, Toshimitsu Kobayashi

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Conclusion. Mitochondrial dysfunction in the cochlea potentiates the ototoxicity of aminoglycosides. Objective. This study examined whether mitochondrial dysfunction in the cochlea affects the ototoxicity of aminoglycosides. Materials and methods. Nineteen guinea pigs were treated with the mitochondrial toxin 3-nitropropionic acid (3-NP), kanamycin, both agents, or normal saline as control. After 14 days, hair cell loss and auditory brainstem response (ABR) were assessed. Results. The administration of 400 mg/kg of kanamycin caused neither hair cell loss nor ABR threshold shift. Administration of 3-NP caused mild ABR threshold shift without significant hair cell loss. Administration of 3-NP and kanamycin caused ABR threshold shift and significant hair cell loss.

Original languageEnglish
Pages (from-to)1280-1285
Number of pages6
JournalActa Oto-Laryngologica
Issue number12
Publication statusPublished - 2008


  • Aminoglycoside
  • Auditory brainstem response
  • Mitochondria
  • Ototoxicity

ASJC Scopus subject areas

  • Otorhinolaryngology


Dive into the research topics of 'Ototoxic interaction of kanamycin and 3-nitropropionic acid'. Together they form a unique fingerprint.

Cite this