Nitric oxide synthase inhibitor reduces noise-induced cochlear damage in guinea pigs

Diao, Mei; Gao, Wenyuan; Sun, Jiayu

doi:10.1080/00016480701242436

Cited by 13 publications

(6 citation statements)

References 15 publications

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“…A previous study reported that NO production decreased when the perilymph was perfused with L-NAME in a noise-induced hearing loss model (12). Similarly, noise-induced increase in the NO levels in the cochlea was significantly attenuated by L-NAME in another study (13). …”

Section: Introductionmentioning

confidence: 72%

N-Acetylcysteine and N-Nitroarginine Methyl Ester Attenuate Carboplatin-Induced Ototoxicity in Dissociated Spiral Ganglion Neuron Cultures

Moon

Kim

Chu

et al. 2011

Clin Exp Otorhinolaryngol

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ObjectivesCarboplatin, a platinum-containing anti-cancer drug used to treat a variety of cancers, induces ototoxicity. Since, reactive oxygen species (ROS) and nitric oxide (NO) seem to be responsible for this toxicity, the antioxidant, N-acetyl-L-cysteine (L-NAC), and NO synthetase inhibitor, N-nitro-L-arginine methyl ester (L-NAME) were predicted to have protective effects against carboplatin ototoxicity. The aim of this study was to test for the protective effects of L-NAC and L-NAME on cochlear hair cells and spiral ganglion neurons (SGNs).MethodsCochlear organotypic cultures and dissociated spiral ganglion neuron cultures, from mice postnatal day 5 cultures were used in this study. The cultures were treated with carboplatin alone or in combination with L-NAC or L-NAME, and carboplatin-induced damage was monitored.ResultsTreatment with carboplatin induced a significant loss of outer hair cells, while inner hair cells were preserved in the cochlear organotypic cultures. Addition of L-NAC or L-NAME reduced the amount of carboplatin-induced hair cell damage; the differences did not reach statistical significance. However, carboplatin significantly decreased the number of surviving SGNs in dissociated cultures. The toxic effects were significantly reduced by addition of L-NAC or L-NAME. In addition, carboplatin induced the loss of neurites from the SGN somata, and this was not blocked with L-NAC or L-NAME.ConclusionThe results of this study suggest that ROS and NO are involved in carboplatin-induced damage to hair cells and SGNs, and administration of L-NAC/L-NAME can be used to attenuate the toxicity.

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Section: Introductionmentioning

confidence: 72%

N-Acetylcysteine and N-Nitroarginine Methyl Ester Attenuate Carboplatin-Induced Ototoxicity in Dissociated Spiral Ganglion Neuron Cultures

Moon

Kim

Chu

et al. 2011

Clin Exp Otorhinolaryngol

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“…Ascorbic acid is a free-radical scavenger that specifically targets reactive oxygen species. L-NAME is a nitric oxide synthase inhibitor, which was demonstrated to be protective against noiseinduced hearing loss in an animal model and to decrease the production of nitric oxide within the perilymph 12,13. LCySSG and ribose-cysteine are both prodrugs for GSH.…”

Section: Methodsmentioning

confidence: 99%

A combination antioxidant therapy prevents age‐related hearing loss in C57BL/6 mice

Heman‐Ackah

Juhn

Huang

et al. 2010

Otolaryngol.--head neck surg.

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“…Numerous studies have indicated that nitration of proteins can be reversed, and targeting nitrative stress is a promising interventional strategy for mitigating oxidative damage to the cochlea [48,52,[56][57][58]. Protein nitration and its signaling have been targeted to prevent apoptosis in organs such as the eye, pancreas, and kidney [59,60].…”

Section: Targeting Nitrative Stress For Otoprotectionmentioning

confidence: 99%

“…Although a direct link between inhibition of nitrative stress with ebselen and attenuation of NIHL is yet to be reported, phase 2 clinical trials in healthy adults aged 18-31 years indicated that 400 mg of ebselen treatment twice daily prevented temporary and permanent noise-induced hearing loss [64]. Treatment of mice with antagonists of nitric oxide synthase such as L-NAME attenuated the noise-induced increase in the level of 3-NT [43,58]. Additionally, compounds such as sodium butyrate, adenosine amine congener (ADAC), polyphenols, Astragaloside IV, L-cysteine, and N-acetyl cysteine (NAC) were reported to prevent cochlear nitrative stress and hearing loss [56,[65][66][67][68][69].…”

Section: Targeting Nitrative Stress For Otoprotectionmentioning

confidence: 99%

Nitrative Stress and Auditory Dysfunction

Shahab

Jamesdaniel

2022

Pharmaceuticals

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Nitrative stress is increasingly recognized as a critical mediator of apoptotic cell death in many pathological conditions. The accumulation of nitric oxide along with superoxide radicals leads to the generation of peroxynitrite that can eventually result in the nitration of susceptible proteins. Nitrotyrosine is widely used as a biomarker of nitrative stress and indicates oxidative damage to proteins. Ototoxic insults, such as exposure to noise and ototoxic drugs, enhance the generation of 3-nitrotyrosine in different cell types in the cochlea. Nitrated proteins can disrupt critical signaling pathways and eventually lead to apoptosis and loss of sensory receptor cells in the cochlea. Accumulating evidence shows that selective targeting of nitrative stress attenuates cellular damage. Anti-nitrative compounds, such as peroxynitrite decomposition catalysts and inducible nitric oxide synthase inhibitors, prevent nitrative stress-mediated auditory damage. However, the role of nitrative stress in acquired hearing loss and its potential significance as a promising interventional target is yet to be fully characterized. This review provides an overview of nitrative stress mechanisms, the induction of nitrative stress in the auditory tissue after ototoxic insults, and the therapeutic value of targeting nitrative stress for mitigating auditory dysfunction.

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Nitric oxide synthase inhibitor reduces noise-induced cochlear damage in guinea pigs

Abstract: Group III showed significantly greater OHC loss, threshold shifts and NO level compared with group I and group IV. Compared with group III, noise-induced elevation in NO level in the cochlea was significantly attenuated by L-NAME (p<0.001).

Cited by 13 publications

References 15 publications

N-Acetylcysteine and N-Nitroarginine Methyl Ester Attenuate Carboplatin-Induced Ototoxicity in Dissociated Spiral Ganglion Neuron Cultures

N-Acetylcysteine and N-Nitroarginine Methyl Ester Attenuate Carboplatin-Induced Ototoxicity in Dissociated Spiral Ganglion Neuron Cultures

A combination antioxidant therapy prevents age‐related hearing loss in C57BL/6 mice

Nitrative Stress and Auditory Dysfunction

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