Abstract
Over the last 10 years new information has been published providing a better understanding of the risk factors, mechanism and prevention of aminoglycoside ototoxicity. The use of a higher dose and once-daily intravenous administration of aminoglycosides has shown clinical effectiveness with no increase in ototoxicity when compared to traditional regimens. An enhanced susceptibility to aminoglycoside cochlear toxicity has been linked to an A-to-G substitution in location 1555 of the mitochondrial ribosomal ribonucleic acid (RNA). More recently, a second mutation involving a thymidine deletion in the 12s ribosomal RNA gene has been identified which can predispose patients to aminoglycoside auditory toxicity. Experimental evidence in animals has indicated that reactive oxygen species are one of the most important factors responsible for the development of aminoglycoside ototoxicity. The animal data has suggested a decrease in hearing loss induced by aminoglycosides when antioxidant or iron chelator therapy is given concomitantly with aminoglycoside antibiotics.
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