Principles in Cochlear Toxicity

Anniko, Matti

doi:10.1007/978-3-642-69928-3_35

Cited by 25 publications

(6 citation statements)

References 59 publications

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“…The findings are also in agreement with human studies [18]. Acoustic and ototoxic insults also typically cause greater damage to OHCs than IHCs [19,20]. One possible explanation of the difference in susceptibility between OHCs and IHCs is based on a number of mor phological differences in the organ of Corti [21].…”

Section: Discussionsupporting

confidence: 82%

Age-Related Degeneration of the Organ of Corti in Two Genotypes of Mice

Hultcrantz

1994

ORL

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Degenerative changes in the organ of Corti were investigated in two genotypes of mice, CBA/Ca (moderate age-related late-onset hearing loss) and C57BL/6J (spontaneous early-onset auditory deterioration), ranging in age from 1 to 21 months (C57BL) and from 1 to 33 months (CBA). Light, transmission and scanning electron microscopes were used for qualitative and quantitative analyses. Alterations of deterioration in the CBA-mouse cochlea showed a late-onset loss of hair cells, lipofuscin in the outer hair cells (OHCs), giant stereocilia on the inner hair cells and elevated pillar heads. In C57BL mice, the primary lesions of the organ of Corti include early damage of stereocilia on OHCs, missing OHCs, and a ruptured reticular lamina. Giant cilia and elevated pillar heads were not evident in C57BL mice. In the aged C57BL mouse cochlea, the whole organ of Corti was collapsed and replaced by the supporting cells, whilst in the oldest CBA mice, completely normal-looking OHCs still remained even in severely deteriorated areas of the organ of Corti. The results indicate that the patterns of degeneration of the organ of Corti are different between CBA/ Ca and C57BL/6J mice, probably under the control of different genes.

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Section: Discussionsupporting

confidence: 82%

Age-Related Degeneration of the Organ of Corti in Two Genotypes of Mice

Hultcrantz

1994

ORL

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“…It has been reported that vestibular endorgans are also damaged by aminoglycoside antibiotics in both animals and humans. Some aminoglycosides(e.g., streptomycin) are more ototoxic to the vestibular organ than to the cochlea 16 . Therefore, vestibular involvement, as well as hearing impairment, would be expected.…”

Section: Discussionmentioning

confidence: 99%

“…The last lane is the molecular weight marker. Lanes 10 to16 are American and Japanese control subjects, and show the normal restriction pattern. Lanes 1 to 9 are patients from five Japanese families with aminoglycoside-induced hearing loss.…”

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confidence: 99%

Genetic and Clinical Features of Sensorineural Hearing Loss Associated With the 1555 Mitochondrial Mutation

et al. 1997

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Five Japanese families showing aminoglycoside-induced hearing loss were genetically as well as clinically investigated. A mitochondrial mutation at nucleotide 1555 was found in 28 out of 32 subjects. One hundred American control subjects did not show any evidence of the mutation at nucleotide 1555, suggesting that the 1555 A-->G (A1555G) mitochondrial mutation may be found more frequently among populations in the Asian continent. Many subjects who harbor this mitochondrial mutation exhibit a mild, high-frequency, progressive hearing loss even without aminoglycoside injection. The results presented here appear to support the hypothesis that the A1555G mutation may play a more general role in causing hearing loss.

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“…Work by Cazals et al (1988) suggests that salicylates may constrict vessels of the spiral lumina, innervated by the sympathetic nervous system. Ototoxic effects influencing the source of production of endolymph (the stria vascularis) become manifest at all sequences at a relatively early stage of salicylate exposure (Anniko 1985). Anniko states that there is a slow elimination rate from the inner ear compared with other tissue compartments in the body, and that the toxicity of drugs seems to be related to tissue binding capacity and saturation of receptor sites.…”

Section: Mechanisms Of Ototoxicitymentioning

confidence: 99%

Ototoxicity Associated with Salicylates

Brien

1993

Drug Safety

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Aspirin, the prototype of the salicylates, is a ubiquitous agent. The availability of aspirin, other salicylates and nonsteroidal anti-inflammatory drugs (NSAIDs) as prescription and over-the-counter medications means there is a wealth of clinical experience with these agents. Among the documented adverse effects of aspirin is the potential for ototoxicity. Tinnitus and hearing loss, usually reversible, are associated with acute intoxication and long term administration of salicylates. A range of measured serum concentrations are reported as correlating with documented ototoxicity (19.6 to > 67 mg/dl). Most case reports are based on total serum salicylate concentrations whereas unbound serum salicylate concentrations appear to reflect more closely the risk of ototoxicity. The pathophysiology of toxicity may be related to biochemical and subsequent electrophysiological changes in the inner ear and eighth cranial nerve impulse transmission. Localised drug accumulation and vasoconstriction in auditory microvasculature may be mediated by the antiprostaglandin activity of these agents. Ototoxicity, although not life-threatening, may add to the morbidity of patients taking salicylates or NSAIDs in therapeutic and toxic doses.

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Principles in Cochlear Toxicity

Cited by 25 publications

References 59 publications

Age-Related Degeneration of the Organ of Corti in Two Genotypes of Mice

Age-Related Degeneration of the Organ of Corti in Two Genotypes of Mice

Genetic and Clinical Features of Sensorineural Hearing Loss Associated With the 1555 Mitochondrial Mutation

Ototoxicity Associated with Salicylates

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