Oxidative Stress in the Cochlea: An Update

Poirrier, Anne‐Lise; Pincemaïl, Joël; Ackerveken, Priscilla Van den; Pj, Lefèbvre; Malgrange, Brigitte

doi:10.2174/092986710792927895

Cited by 136 publications

(81 citation statements)

References 230 publications

(258 reference statements)

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“…To date, increased ROS has been shown to lead to spiral and vestibular ganglion cell death [Takumida et al, 2003;Jeong et al, 2010;Poirrier et al, 2010]. In this study, MsrA, MsrB1 and MsrB2 were expressed in ganglion cells of both cochlea and vestibule.…”

Section: +mentioning

confidence: 66%

Methionine Sulfoxide Reductase A, B1 and B2 Are Likely to Be Involved in the Protection against Oxidative Stress in the Inner Ear

Kwon

Oh²,

Kim³

et al. 2014

Cells Tissues Organs

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The methionine sulfoxide reductase (Msr) family of proteins is a class of repair enzymes that reduce methionine-S (MsrA) or methionine-R (MsrB) sulfoxide to methionine. Recent studies have reported that mutations in the MSRB3 gene cause autosomal recessive hearing loss in humans, and in mice MsrB3 deficiency leads to profound hearing loss due to hair cell apoptosis and stereocilia degeneration. However, apart from MsrB3, studies on Msr proteins in the inner ear have not yet been reported. In this study, we identified and characterized Msr expression in the cochlea and vestibule. First, we confirmed RNA expression levels of Msr family members in the cochlea and vestibule using reverse transcription PCR and detected Msr family members in both tissues. We also conducted immunohistochemical staining to localize Msr family members within the cochlea and vestibule. In the cochlea, MsrA was detected in supporting cells, spiral ligament, spiral limbus, Reissner's membrane and the spiral ganglion. MsrB1 was specifically expressed in hair cells and the spiral ganglion. MsrB2 was noted in the spiral ganglion, tectorial membrane and stria vascularis. In the vestibule, MsrA and MsrB1 were detected in hair cells and the vestibular ganglion, while MsrB2 was restricted to the vestibular ganglion. In this study, we identified distinct distributions of Msr family members in the organ of Corti and hypothesized that MsrA, MsrB1 and MsrB2 protect proteins in the organ of Corti from oxidative stress.

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Section: +mentioning

confidence: 66%

Methionine Sulfoxide Reductase A, B1 and B2 Are Likely to Be Involved in the Protection against Oxidative Stress in the Inner Ear

Kwon

Oh²,

Kim³

et al. 2014

Cells Tissues Organs

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“…Cisplatin has been shown to enhance the formation of reactive oxygen species, and the free radicalinduced cell damage is thought to play an important role in cisplatin neurotoxicity (Dehne et al, 2001;Poirrier et al, 2010). Although cisplatin is known to be neurotoxic and is believed to exacerbate the impact of the peripheral cisplatin-induced ototoxicity, its effects on the central auditory system are not well characterized.…”

Section: Introductionmentioning

confidence: 99%

d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

Gopal

Shrestha

et al. 2012

Neurotoxicology and Teratology

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Cisplatin is a platinum-based chemotherapeutic agent widely used for the treatment of various types of cancer. Patients undergoing cisplatin treatment often suffer from a condition known as "chemobrain", ototoxicity, peripheral neuropathy, weight loss, nausea, vomiting, nephrotoxicity, seizures, hearing loss and tinnitus.D-Methionine (D-Met), a sulfur-containing nucleophilic antioxidant, has been shown to prevent cisplatininduced side effects in animals without antitumor interference. In this study, we have used an in vitro model of cortical networks (CNs), enriched in auditory cortex cells; to quantify cisplatin neurotoxicity and the protective effects of D-Met. Dissociated neurons from auditory cortices of mouse embryos were grown on microelectrode arrays with 64 transparent indium-tin oxide electrodes, which enabled continuous optical and electrophysiological monitoring of network neurons. Cisplatin at 0.10-0.25 mM induced up to a 200% increase in spontaneous spiking activity, while concentrations at or above 0.5 mM caused irreversible loss of neuronal activity, accompanied by cell death. Pretreatment with D-Met, at a concentration of 1.0 mM, prevented the cisplatin-induced excitation at 0.10-0.25 mM, caused sustained excitation without occurrence of cell death at 0.5 mM, and delayed cell death at 0.75 mM cisplatin. L-Methionine, the optical isomer, showed lower potency and less efficacy than D-Met, was less protective against 0.1 mM cisplatin, and proved ineffective at a concentration of 0.5 mM cisplatin. Pre-exposure time of D-Met was associated with the protective effects at 0.1 and 0.5 mM cisplatin, with longer pre-exposure times exhibiting better protection. This study quantifies as a function of concentration and time that D-Met protects central nervous system tissue from acute cisplatin toxicity.

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“…A number of the oxidation products of polyunsaturated fatty acids (PUFA) in phospholipids act as mediators of apoptosis. ROS activate apoptotic or necrotic intracellular pathways, including the c-Jun N-terminal kinase (JNK) pathway (15). The inhibition of the JNK pathway has been demonstrated to help hair cells injured by aminoglycosides (15).…”

Section: Use Of Cape In Antibiotic-induced Ototoxicitymentioning

confidence: 99%

“…ROS activate apoptotic or necrotic intracellular pathways, including the c-Jun N-terminal kinase (JNK) pathway (15). The inhibition of the JNK pathway has been demonstrated to help hair cells injured by aminoglycosides (15). Due to the fact that the trigger mechanism starts with ROS activation, CAPE may be a promising agent to block this cascade at two different points (Fig.…”

Section: Use Of Cape In Antibiotic-induced Ototoxicitymentioning

confidence: 99%

Future opportunities in preventing ototoxicity: Caffeic acid phenethyl ester may be a candidate (Review)

Akyol

Işık

Altuntaş

et al. 2015

Molecular Medicine Reports

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Oxidative Stress in the Cochlea: An Update

Cited by 136 publications

References 230 publications

Methionine Sulfoxide Reductase A, B1 and B2 Are Likely to Be Involved in the Protection against Oxidative Stress in the Inner Ear

Methionine Sulfoxide Reductase A, B1 and B2 Are Likely to Be Involved in the Protection against Oxidative Stress in the Inner Ear

d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

Future opportunities in preventing ototoxicity: Caffeic acid phenethyl ester may be a candidate (Review)

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