Aminoglycoside induced ototoxicity

Guthrie, O’neil W.

doi:10.1016/j.tox.2008.04.015

Cited by 225 publications

(170 citation statements)

References 61 publications

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“…Previous studies on predisposing factors for aminoglycoside ototoxicity point to drug-drug interaction, 9,10 underlying medical conditions, 11 and stress. 12 Comorbid conditions, such as perinatal asphyxia, hypovolemia, shock, or sepsis, were supposed to augment aminoglycoside ototoxicity.…”

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confidence: 99%

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Kao

Tsai

Lai

et al. 2011

Laboratory Investigation

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Aminoglycoside ototoxicity is a common cause of drug-induced hearing loss. Toxicity is dose related, but some patients may still develop hearing loss even under safe dosage. Apart for genetic idiosyncrasy, indirect evidences imply that ischemia may increase the aminoglycoside ototoxic sensitivity because common clinical situations associated with cochlear ischemia such as noise, sepsis, and shock are known to augment the development of aminoglycoside ototoxicity. At present, a direct interaction of cochlear ischemia and aminoglycoside ototoxicity is still lacking. This study demonstrated a direct evidence of increased gentamicin (GM) ototoxic sensitivity in chronic guinea pig models of transient cochlear ischemia. No permanent auditory changes were observed after a single dose of GM (125 mg/kg) or after transient cochlear ischemia for 30 min. Persistent and significant auditory threshold shift was detected when GM was given after transient cochlear ischemia. Cochlear hair cells and spiral ganglion neurons are the major regions affected. Apoptosis contributes to hair cell death during acute interaction of ischemia and GM ototoxicity. Increased apoptotic cell death was also depicted when GM crossreacted with hypoxia in vitro, using cochlear cell lines. Generation of reactive oxygen species, loss of mitochondrial membrane potential, calcium release, and caspase-dependent apoptotic cell death were shown during the interaction of hypoxia and GM ototoxicity in vitro. This synergistic ototoxicity may be critical to aminoglycoside-induced hearing loss in clinical scenarios. The results should improve our understanding of the interacting mechanism and potential preventive strategy to aminoglycoside ototoxicity.

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confidence: 99%

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Kao

Tsai

Lai

et al. 2011

Laboratory Investigation

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“…Strial degeneration has been reported previously, but the authors were unsure whether it was a secondary or primary effect of aminoglycoside treatment. 4,33 The connective tissue cells of the spiral limbus are highly susceptible to ototoxicity. At the same time, the spiral limbus may serve as one of the most sensitive indicators of changes in the chemical composition of perilymph.…”

Section: Figmentioning

confidence: 99%

“…4 Recently, the beneficial effect of platelet-rich plasma and neural-induced human mesenchymal stem cells was demonstrated on axonal regeneration from a facial nerve axotomy injury in a guinea pig model. 37 Although a significantly protective effect was observed in three guinea pig ganglion cells, according to immunohistochemical examination, the current study did not show therapeutic or protective effects of autologous serum in ganglion cells.…”

Section: Figmentioning

confidence: 99%

“…The degeneration of nerve fibres, spiral ganglion neurons and supporting cells is secondary to hair cell damage. 3,4 Many reports have discussed possible prevention methods for ototoxicity, such as anti-inflammatory drugs, antioxidants, apoptosis inhibitors, neuroprotective compounds, neurotrophic factors and gene therapeutic approaches. 2,5,6 In recent decades, stem cells have also been used to replace deficient cell types in order to restore hearing.…”

Section: Introductionmentioning

confidence: 99%

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Therapeutic and protective effects of autologous serum in amikacin-induced ototoxicity

et al. 2017

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Objective: Possible therapeutic and protective benefits of intratympanic autologous serum application in amikacininduced ototoxicity were investigated.Methods: Twenty-four guinea pigs were separated equally into two groups: therapeutic (group A) and protective (group B). Transient evoked otoacoustic emissions were recorded before and after autologous serum application. Apoptotic cells were identified in the organ of Corti, spiral limbus and spiral ganglion by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling ('TUNEL') method.Results: Transient evoked otoacoustic emission responses at 1, 1.4 and 2.8 kHz improved without significance after autologous serum application in group A ( p > 0.05). A significantly protective effect of autologous serum was determined at 4 kHz in group B ( p < 0.05). There were significantly fewer apoptotic cells at the spiral limbus in the therapeutic and protective groups compared to the control group ( p < 0.05).Conclusion: Autologous serum may offer protection against ototoxicity-induced hearing loss, but it cannot restore hearing. Immunohistochemically, autologous serum significantly decreases activation of the intrinsic pathway of pro-apoptotic signalling in mesenchymal cells compared to neurons and neurosensory cells.

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“…This listening behavior appears to increase neural activity corresponding to the intact ear and, at the same time, reduce neural connections between the affected cochlea and auditory cortex 22 . In order to prevent this maladaptive cortical change induced by 'non-use', it appears to be beneficial for SSHL patients to perform 'constraint-induced sound therapy (CIST) , head trauma, autoimmune inner ear disease 8,9 , Cogan's syndrome 27,28 , genetic diseases 29 , ototoxic drugs 30 , retrocochlear disorders related to vestibular schwannoma 31 , auditory neuropathy 32 , or stroke 33 .…”

Section: Introductionmentioning

confidence: 99%

Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss

Sekiya

Fukushima

Teismann

et al. 2016

JoVE

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Sudden sensorineural hearing loss (SSHL) is characterized by acute, idiopathic hearing loss. The estimated incidence rate is 5-30 cases per 100,000 people per year. The causes of SSHL and the mechanisms underlying SSHL currently remain unknown. Based on several hypotheses such as a circulatory disturbance to the cochlea, viral infection, and autoimmune disease, pharmaco-therapeutic approaches have been applied to treat SSHL patients; however, the efficacy of the standard treatment, corticosteroid therapy, is still under debate. Exposure to intense sounds has been shown to cause permanent damage to the auditory system; however, exposure to a moderate level enriched acoustic environment after noise trauma may reduce hearing impairments. Several neuroimaging studies recently suggested that the onset of SSHL induced maladaptive cortical reorganization in the human auditory cortex, and that the degree of cortical reorganization in the acute SSHL phase negatively correlated with the recovery rate from hearing loss. This article reports the development of a novel neuro-rehabilitation approach for SSHL, "constraint-induced sound therapy (CIST)". The aim of the CIST protocol is to prevent or reduce maladaptive cortical reorganization by using an enriched acoustic environment. The canal of the intact ear of SSHL patients is plugged in order to motivate them to actively use the affected ear and thereby prevent progress of maladaptive cortical reorganization. The affected ear is also exposed to music via a headphone for 6 hr per day during hospitalization. The CIST protocol appears to be a safe, easy, inexpensive, and effective treatment for SSHL.

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Aminoglycoside induced ototoxicity

Cited by 225 publications

References 61 publications

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Transient ischemia/hypoxia enhances gentamicin ototoxicity via caspase-dependent cell death pathway

Therapeutic and protective effects of autologous serum in amikacin-induced ototoxicity

Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss

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