Influence of intense sound exposure on glutathione synthesis in the cochlea

Yamasoba, Tatsuya; Harris, Craig; Shoji, Fumi; Lee, Rosanna J.; Nuttall, Alfred L.; Miller, Josef M.

doi:10.1016/s0006-8993(98)00660-x

Cited by 80 publications

(61 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As stated earlier, evidence for noise-induced generation of ROS/NO in the cochlea comes from the findings that noise exposure increases the levels of hydroxyl radicals in cochlear fluids (2), superoxide anion radicals (24), and glutathione in the stria vascularis (25) and NO in the cochlear lateral wall (26). Previous studies on NOS in the cochlea demonstrated that whereas much less NOS activity is observed in the organ of Corti (27), nNOS (NOS1) and eNOS (NOS3) are located constitutively in the modiolar core and lateral wall, respectively (28).…”

Section: Discussionmentioning

confidence: 99%

Mechanism Underlying the Protective Effect of Tempol and Nω-Nitro-L-arginine Methyl Ester on Acoustic Injury: Possible Involvement of c-Jun N-Terminal Kinase Pathway and Connexin26 in the Cochlear Spiral Ligament

et al. 2010

View full text Add to dashboard Cite

Abstract. There is evidence that reactive oxygen species (ROS) are formed in the cochlea during acoustic injury. However, very little is known about the involvement of ROS signals in the spiral ligament (SL) during such injury. The purpose of this study was to determine the effect of the multifunctional antioxidant tempol and the nitric oxide synthase inhibitor N ω -nitro-L-arginine methyl ester (L-NAME) on acoustic injury and the c-Jun N-terminal kinase (JNK) pathway in the SL. Exposure of adult mice to noise (8-kHz octave band, 110-dB SPL for 1 h) produced permanent hearing loss. Noise exposure increased not only the formation of a protein modified by 4-hydroxynonenal and formation of nitrotyrosine, but also the level of phospho-JNK in the SL. Pretreatment with tempol or L-NAME was effective in protecting the noise-exposed animals from hearing loss, as well as in abolishing the noise-induced activation of the JNK signaling pathway. Interestingly, noise exposure caused a dramatic decrease in connexin26 level in the SL. This decrease was prevented by tempol or L-NAME. Taken together, our data suggest that noise-induced hearing loss is due at least in part to ROS / nitric oxide-mediated activation of the JNK pathway and down-regulation of connexin26 in the SL of mice.

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanism Underlying the Protective Effect of Tempol and Nω-Nitro-L-arginine Methyl Ester on Acoustic Injury: Possible Involvement of c-Jun N-Terminal Kinase Pathway and Connexin26 in the Cochlear Spiral Ligament

et al. 2010

View full text Add to dashboard Cite

show abstract

“…This can be an indicator for oxidative stress in textile workers exposed to long-term continuous noise. According to the reports which showed that the level of free radical increased in cochlea by acoustic stimulation, the significant increase in MDA level 7,8) and evident hearing loss in textile workers compared to controls suggested that oxidative stress caused by noise exposure in cochlea may lead to hearing impairment.…”

Section: Discussionmentioning

confidence: 99%

“…Decreases in CAT and SOD activities may be due to this consumption. In some experimental studies on noise-related hearing loss, it has been reported that oxidative stress caused by reduction in antioxidant enzymes or substances may be attenuated by giving exogenous antioxidants 8,18,[23][24][25] . If it could be proven that there is a strong association between noiserelated hearing loss and oxidative stress, then some exogenous antioxidant therapies may have merit in the prevention and /or treatment of noise-related hearing loss.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Effects of Noise on Hearing and Oxidative Stress in Textile Workers

et al. 2007

View full text Add to dashboard Cite

“…γ-GCS is considered to be a candidate of target genes for the AP-1 over-expressed in the cochlea after noise exposure. Indeed, the GSH level is significantly increased in the lateral wall 2 and 4 h after intense noise exposure and returns to normal 6 h post-exposure (16). However, this increase is not seen in the sensory epithelium and modiolus.…”

Section: +mentioning

confidence: 91%

Transcriptional Factors in the Cochlea Within the Inner Ear

et al. 2005

View full text Add to dashboard Cite

Abstract. Differential regulation of gene expression by transcription factors is widely viewed as one of the principal mechanisms guiding development. Although numerous DNA binding proteins have been identified in various tissues, the role of individual transcription factors in the differentiation of specific cell groups, such as those populating the inner ear, is just beginning to be elucidated. It is known that transcription factors are induced in response to many signals that lead to cell growth, differentiation, inflammatory responses, the regulation of apoptosis, and neoplastic transformation. There are various transcription factors in the cochlea of the inner ear. These include activator protein-1 and nuclear factor-kappa B, glucocorticoid receptor, and so on. Based on recent reports and our investigation, in this article we review possible functions and expression of these transcription factors.

show abstract

Influence of intense sound exposure on glutathione synthesis in the cochlea

Cited by 80 publications

References 26 publications

Mechanism Underlying the Protective Effect of Tempol and Nω-Nitro-L-arginine Methyl Ester on Acoustic Injury: Possible Involvement of c-Jun N-Terminal Kinase Pathway and Connexin26 in the Cochlear Spiral Ligament

Mechanism Underlying the Protective Effect of Tempol and Nω-Nitro-L-arginine Methyl Ester on Acoustic Injury: Possible Involvement of c-Jun N-Terminal Kinase Pathway and Connexin26 in the Cochlear Spiral Ligament

The Effects of Noise on Hearing and Oxidative Stress in Textile Workers

Transcriptional Factors in the Cochlea Within the Inner Ear

Contact Info

Product

Resources

About