The clinical utility of the aminoglycoside antibiotics is hampered by their well-known capacity to cause labyrinthine and renal damage. The mechanism by which these damages are produced is unknown. Attention was focused on the aminosugar moiety of these antibiotics by the finding of Owada (1962) which demonstrated that 3-aminoglucose is as ototoxic as its parent antibiotic, kanamycin. It is known that aminosugars compete with glucose for transport and that the sensory cells of the cochlea depend on glucose as a primary energy source. The hypothesis that grew out of these considerations was that kanamycin might be causing its ototoxicity by inhibiting glucose transport at one of several sites in the inner ear. To test this hypothesis the ototoxicity of kanamycin was determined in hyperglycemic animals. Hyperglycemia clearly and dramatically protects animals against ototoxicity as evidenced both by electrocochleographical and histological examination.