A molecular and cellular hypothesis for aminoglycoside-induced deafness.

The ototoxic effects of aminoglycoside antibiotics are well known. However, a molecular and cellular mechanism for the death of cochlear hair cells has remained difficult to prove. Human genetic studies have shown that a rare trait for hypersensitivity to aminoglycosides is conferred by mitochondrial genetic variation. Recently, a gene involved has been identified as the mitochondrial small ribosomal RNA gene, consistent with the known mechanism of aminoglycoside action against bacteria. We used the existing data as a basis for our hypothesis of a molecular and cellular model for aminoglycoside ototoxicity that is described in this paper.