1. Aminoglycoside-induced ototoxicity.
- Author
-
Selimoglu E
- Subjects
- Aminoglycosides administration & dosage, Aminoglycosides toxicity, Animals, Anti-Bacterial Agents toxicity, Dose-Response Relationship, Drug, Drug Administration Schedule, Genetic Predisposition to Disease, Genetic Testing, Hair Cells, Auditory drug effects, Hearing Disorders genetics, Hearing Disorders prevention & control, Humans, Incidence, Meniere Disease drug therapy, Mutation, RNA genetics, RNA, Mitochondrial, RNA, Ribosomal genetics, Risk Assessment, Risk Factors, Aminoglycosides adverse effects, Anti-Bacterial Agents adverse effects, Cochlea drug effects, Hearing Disorders chemically induced, Vestibule, Labyrinth drug effects
- Abstract
It has long been known that the major irreversible toxicity of aminoglycosides is ototoxicity. Among them, streptomycin and gentamicin are primarily vestibulotoxic, whereas amikacin, neomycin, dihydrosterptomycin, and kanamicin are primarily cochleotoxic. Cochlear damage can produce permanent hearing loss, and damage to the vestibular apparatus results in dizziness, ataxia, and/or nystagmus. Aminoglycosides appear to generate free radicals within the inner ear, with subsequent permanent damage to sensory cells and neurons, resulting in permanent hearing loss. Two mutations in the mitochondrial 12S ribosomal RNA gene have been previously reported to predispose carriers to aminoglycoside-induced ototoxicity. As aminoglycosides are indispensable agents both in the treatment of infections and Meniere's disease, a great effort has been made to develop strategies to prevent aminoglycoside ototoxicity. Anti-free radical agents, such as salicylate, have been shown to attenuate the ototoxic effects of aminoglycosides. In this paper, incidence, predisposition, mechanism, and prevention of aminoglycoside-induced ototoxicity is discussed in the light of literature data.
- Published
- 2007
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