Protective effect of edaravone against tobramycin-induced ototoxicity

Asplund, Monika Stenkvist; Lidian, Adnan; Linder, Birgitta; Takumida, Masaya; Anniko, Matti

doi:10.1080/00016480802008199

Cited by 17 publications

(14 citation statements)

References 23 publications

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“…Also, various studies show that potential free radical scavengers, such as α-tocopherol (vitamin E) and α-lipoic acid, inhibit gentamicin ototoxicity by neutralizing the free radicals [30,36]. The antioxidant agent, edaravone, which is used particularly in the treatment of acute myocardial infarction, was found effective at inhibiting streptomycin and tobramycin ototoxicity [37,38]. In addition, protection from gentamicin ototoxicity was found in agent M40403, which has a similar efficacy as SOD [39].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Protective Effect of Beta Glucan on Amikacin Ototoxicity Using Distortion Product Otoacoustic Emission Measurements in Rats

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et al. 2013

Clin Exp Otorhinolaryngol

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ObjectivesThis experimental study investigated the possible protective effect of beta glucans on amikacin ototoxicity.MethodsThirty-eight rats with normal distortion product otoacoustic emissions (DPOAEs) were divided into four groups. Group K was the control group. Group A was injected intramuscularly (i.m.) with amikacin 600 mg/kg/day between days 1-15. Group AB was given beta glucan gavage 1 mg/kg/day on days 0-15 and given amikacin 600 mg/kg/day i.m. on days 1-15. Group B was administered only beta glucan gavage, 1 mg/kg/day, on days 0-15. The DPOAEs were elicited in different frequency regions between 2,003 and 9,515 Hz, as distortion product diagrams (DPgrams), before and after the medication was administered, in all groups, on days 1, 5, 10, and 15.ResultsNo significant changes in the DPgrams were observed in group K. In group A, significant deterioration was observed at the 8,003 and 9,515 Hz frequencies on day 10, and at the 3,991, 4,557, 5,660, 6,726, 8,003, and 9,515 Hz frequencies on day 15. For group AB, statistically significant deterioration was observed at the 2,824, 8,003, and 9,515 Hz frequencies on day 15. The results for group B showed a significant improvement of hearing at the 2,378, 2,824, 3,363, and 3,991 Hz frequencies on day 1, at the 3,363, 3,991, and 8,003 Hz frequencies on day 10, and at the 8,003 Hz frequency on day 15.ConclusionThis study suggests that amikacin-induced hearing loss in rats may be limited to some extent by concomitant use of beta glucan.

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Section: Discussionmentioning

confidence: 99%

Evaluation of the Protective Effect of Beta Glucan on Amikacin Ototoxicity Using Distortion Product Otoacoustic Emission Measurements in Rats

Bayındır

Filiz

Iraz

et al. 2013

Clin Exp Otorhinolaryngol

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“…Edaravone (MCI-186, 3-methyl-1-phenyl-pyrazolin-5-one) which is clinically used to treat acute cerebral infarction and acute myocardial infarction (Mishina et al, 2005;Tsujita et al, 2004) is a free radical scavenger and can interact with both peroxyl and hydroxyl radicals to form oxidized compounds (Asplund et al, 2009). Edaravone is reported to reduce the amount of oxidative DNA damage and lipid peroxidation in barotraumatic inner ear (Maekawa et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Protective role of edaravone against cisplatin-induced ototoxicity in an auditory cell line

Chang

Lee

et al. 2015

Hearing Research

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“…It can interact with both peroxyl and hydroxyl radicals to form oxidized compounds and thus attenuate ischemic damage [12]. Many studies have revealed that free radical scavengers are also very useful in the treatment of otology disorders, such as inner ear barotrauma, aminoglycoside-induced ototoxicity, and cisplatin-induced ototoxicity [13–15].…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Edaravone on Glutamate-Induced Neurotoxicity in Spiral Ganglion Neurons

et al. 2016

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Glutamate is an important excitatory neurotransmitter in mammalian brains, but excessive amount of glutamate can cause “excitotoxicity” and lead to neuronal death. As bipolar neurons, spiral ganglion neurons (SGNs) function as a “bridge” in transmitting auditory information from the ear to the brain and can be damaged by excessive glutamate which results in sensorineural hearing loss. In this study, edaravone, a free radical scavenger, elicited both preventative and therapeutic effects on SGNs against glutamate-induced cell damage that was tested by MTT assay and trypan blue staining. Ho.33342 and PI double staining revealed that apoptosis as well as necrosis took place during glutamate treatment, and apoptosis was the main type of cell death. Oxidative stress played an important role in glutamate-induced cell damage but pretreatment with edaravone alleviated cell death. Results of western blot demonstrated that mechanisms underlying the toxicity of glutamate and the protection of edaravone were related to the PI3K pathway and Bcl-2 protein family.

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Protective effect of edaravone against tobramycin-induced ototoxicity

Cited by 17 publications

References 23 publications

Evaluation of the Protective Effect of Beta Glucan on Amikacin Ototoxicity Using Distortion Product Otoacoustic Emission Measurements in Rats

Evaluation of the Protective Effect of Beta Glucan on Amikacin Ototoxicity Using Distortion Product Otoacoustic Emission Measurements in Rats

Protective role of edaravone against cisplatin-induced ototoxicity in an auditory cell line

Protective Effect of Edaravone on Glutamate-Induced Neurotoxicity in Spiral Ganglion Neurons

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