Ototoxic interaction of kanamycin and 3-nitropropionic acid

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.