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      Effect of Isoflurane on the Hearing in Mice

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          Abstract

          Background and Objectives

          The aim of this study was to investigate the relationship between inhalation anesthetics and hearing in mice.

          Materials and Methods

          As inhalation anesthetics, isoflurane was used. Auditory brainstem response and distortion product otoacoustic emission were used as measurement of hearing. Mice were divided into 2 groups. 'Isoflurane group' consisted of mice that were anesthetized with an inspired concentration of 2.0 vol% isoflurane with 2 L/min of oxygen (n=10). 'Control group' consisted of mice that were anesthetized with ketamine and xylazine (n=10).

          Results

          Auditory brainstem response thresholds in mice anesthetized with ketamine and xylazine was not different from those in mice anesthetized with isoflurane. Threshold of DPOAE was higher in mice with isolurane than with ketamine and xylazine. Changes of efferent control may be induced by isoflurane and consequently change the threshold of DPOAE in mice.

          Conclusions

          These results infer that, there was a change of central nervous system induced by inhalation anesthetics, this change also can be applied to the strategies for prevention of hearing loss.

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          Antioxidants attenuate gentamicin-induced free radical formation in vitro and ototoxicity in vivo: D-methionine is a potential protectant.

          Su-Hua Sha, Jochen Schacht (2000)
          We have recently suggested antioxidant therapy against aminoglycoside-induced hearing loss based on the hypothesis of a redox-active aminoglycoside-iron complex causing ototoxicity. The present study compares seven antioxidants and iron chelators for their ability to attenuate gentamicin-induced free radical generation in vitro and ototoxicity in guinea pig in vivo. Free radical formation by gentamicin was measured by chemiluminescence detection both in a non-enzymatic system in vitro and in cell culture. Deferoxamine, 2,3-dihydroxybenzoate, or salicylic acid suppressed gentamicin-induced luminescence in both tests. This indicated the usefulness of the assay as a screen for potential protectants since these agents had previously been shown to attenuate gentamicin-induced ototoxicity in vivo. Histidine and D-methionine, amino acids with chelating and antioxidant properties, also suppressed gentamicin-mediated luminosity both in vitro and in cell culture. In contrast, the metal chelators succimer (2, 3-dimercaptosuccinic acid (DMSA)) and trientine (N, N'-bis[2-aminoethyl]-1,2 ethanediamine) promoted free radical formation and were excluded from further studies. Histidine and D-methionine were then administered to guinea pigs receiving concurrent treatment with gentamicin (120 mg/kgx19 days). Threshold shifts induced by gentamicin were significantly attenuated by twice-daily injections of D-methionine. Once-daily injections of histidine or D-methionine were less effective, pointing to the importance of pharmacokinetics in antioxidant protection in vivo. The study presents a simple screening system for agents with the potential to attenuate gentamicin-induced hearing loss. It also supports the hypothesis of free radical formation as an underlying cause of gentamicin ototoxicity.
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            Overview of mechanical damage to the inner ear: noise as a tool to probe cochlear function.

            Norma Slepecky (1986)
            The majority of experiments causing mechanical damage to the cochlea involve the use of sound pressure waves to cause overstimulation. This presentation is an overview of the research during the past years on the structural damage produced by noise. The effect of noise on the cochlea depends on the type of noise exposure-impulse or continuous. Experiments have been conducted to determine the effect of increasing intensity, the effect of increasing duration, and the effect of equal energy presented over varying periods of time. The initial mechanism of damage, the progression of damage over time, and the ability of hair cells to recover are discussed. Noise has been used as a tool to probe cochlear function by selectively damaging regions along the length of the sensory epithelium and by selectively damaging one of the two types of hair cells. Results obtained from these types of experiments have given us information on cochlear mechanics, as well as of stereocilia micromechanics and transduction. Information on susceptibility of hair cells to noise confirms previous results, suggesting the presence of structural and metabolic gradients both longitudinally and radially within the sensory epithelium. Moreover, noise lesions have been used to map the afferent innervation pattern to the cochlear nucleus, and noise studies show correlation of hair cell damage with efferent innervation pattern.
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              Formation of reactive oxygen species following bioactivation of gentamicin.

              Veronika J. Schacht, S Sha (1999)
              The present study investigated the ability of gentamicin to catalyze free radical reactions and probed the underlying mechanisms by hydroethidine imaging, oxygen consumption, and reduction of cytochrome c. In Epstein-Barr virus-transformed lymphoblastoid cells, a respiratory burst was induced by phorbol ester and detected by hydroethidine, a fluorescent indicator of superoxide radical. The addition of gentamicin increased the fluorescence two-fold while gentamicin did not produce fluorescence in the absence of phorbol ester. In membrane preparations, gentamicin did not enhance NADPH consumption ruling out a direct activation of NADPH oxidase. The formation of reactive oxygen species by gentamicin was additionally supported by experiments that showed gentamicin increased oxygen consumption two-fold in intact cells and a cell-free system. In addition, generation of superoxide was indicated by the gentamicin-stimulated reduction of cytochrome c. The stimulation by gentamicin depended upon the presence of iron (FeII/FeIII) and of arachidonic acid as an electron donor. These results support the hypothesis that an iron-gentamicin complex can increase reactive oxygen species in nonenzymatic and in biological systems. The requirement for a reductive activation in intact cells (e.g., by a respiratory burst) is interpreted as the conversion of an inactive FeIII-gentamicin to a redox-active FeII-gentamicin complex.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Korean J Audiol
                Journal ID (iso-abbrev): Korean J Audiol
                Journal ID (publisher-id): KJA
                Title: Korean Journal of Audiology
                Publisher: The Korean Audiological Society
                ISSN (Print): 2092-9862
                ISSN (Electronic): 2093-3797
                Publication date (Print): April 2012
                Publication date (Electronic): 30 April 2012
                Volume: 16
                Issue: 1
                Pages: 14-17
                Affiliations
                [1 ]Department of Anesthesiology and Pain Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
                [2 ]Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
                Author notes
                Address for correspondence: Jong Woo Chung, MD, PhD. Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 138-736, Korea. Tel +82-2-3010-3718, Fax +82-2-489-2773, jwchung@ 123456amc.seoul.kr
                Article
                DOI: 10.7874/kja.2012.16.1.14
                PMC ID: 3936527
                SO-VID: 5a2f5504-cbbd-4156-abcf-00226a1e639e
                Copyright © Copyright © 2012 The Korean Audiological Society
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 November 2011
                Date revision received : 20 December 2011
                Date accepted : 03 January 2012
                Categories
                Subject: Original Article

                Keywords: hearing,anesthetics,central nervous system,efferent control
                Data availability:
                Keywords: hearing, anesthetics, central nervous system, efferent control

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