scholarly journals Editorial: Sensory Hair Cell Death and Regeneration

2016 ◽  
Vol 10 ◽  
Author(s):  
Michael E. Smith ◽  
Andrew K. Groves ◽  
Allison B. Coffin
Keyword(s):  
Cell Death ◽  
Hair Cell ◽  
Sensory Hair ◽  
Hair Cell Death ◽  
Sensory Hair Cell

scholarly journals Dimethyl Sulfoxide (DMSO) Exacerbates Cisplatin-induced Sensory Hair Cell Death in Zebrafish (Danio rerio)

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e55359 ◽  
Author(s):  
Phillip M. Uribe ◽  
Melissa A. Mueller ◽  
Julia S. Gleichman ◽  
Matthew D. Kramer ◽  
Qi Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Hair Cell ◽  
Dimethyl Sulfoxide ◽  
Danio Rerio ◽  
Sensory Hair ◽  
Hair Cell Death ◽  
Sensory Hair Cell

scholarly journals Sensory hair cell death and regeneration in fishes

2015 ◽  
Vol 9 ◽  
Author(s):  
Jerry D. Monroe ◽  
Gopinath Rajadinakaran ◽  
Michael E. Smith
Keyword(s):  
Cell Death ◽  
Hair Cell ◽  
Sensory Hair ◽  
Hair Cell Death ◽  
Sensory Hair Cell

scholarly journals Oral Antioxidant Vitamins and Magnesium Limit Noise-Induced Hearing Loss by Promoting Sensory Hair Cell Survival: Role of Antioxidant Enzymes and Apoptosis Genes

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1177
Author(s):  
Juan C. Alvarado ◽  
Verónica Fuentes-Santamaría ◽  
Pedro Melgar-Rojas ◽  
María C. Gabaldón-Ull ◽  
José J. Cabanes-Sanchis ◽  
...  
Keyword(s):  
Cell Death ◽  
Hearing Loss ◽  
Antioxidant Enzymes ◽  
Oral Administration ◽  
Hair Cell ◽  
Cell Survival ◽  
Sensory Cell ◽  
Auditory Function ◽  
Sensory Hair ◽  
Sensory Hair Cell

Noise induces oxidative stress in the cochlea followed by sensory cell death and hearing loss. The proof of principle that injections of antioxidant vitamins and Mg2+ prevent noise-induced hearing loss (NIHL) has been established. However, effectiveness of oral administration remains controversial and otoprotection mechanisms are unclear. Using auditory evoked potentials, quantitative PCR, and immunocytochemistry, we explored effects of oral administration of vitamins A, C, E, and Mg2+ (ACEMg) on auditory function and sensory cell survival following NIHL in rats. Oral ACEMg reduced auditory thresholds shifts after NIHL. Improved auditory function correlated with increased survival of sensory outer hair cells. In parallel, oral ACEMg modulated the expression timeline of antioxidant enzymes in the cochlea after NIHL. There was increased expression of glutathione peroxidase-1 and catalase at 1 and 10 days, respectively. Also, pro-apoptotic caspase-3 and Bax levels were diminished in ACEMg-treated rats, at 10 and 30 days, respectively, following noise overstimulation, whereas, at day 10 after noise exposure, the levels of anti-apoptotic Bcl-2, were significantly increased. Therefore, oral ACEMg improves auditory function by limiting sensory hair cell death in the auditory receptor following NIHL. Regulation of the expression of antioxidant enzymes and apoptosis-related proteins in cochlear structures is involved in such an otoprotective mechanism.

scholarly journals Oral Antioxidant Vitamins and Magnesium Limit Noise-induced Hearing Loss by Promoting Sensory Hair Cell Survival: Role of Antioxidant Enzymes and Apoptosis Genes

2020 ◽  
Author(s):  
Juan C Alvarado ◽  
Veronica Fuentes-Santamaría ◽  
Pedro Melgar-Rojas ◽  
Maria C Gabaldon-Ull ◽  
Jose J Cabanes-Sanchis ◽  
...  
Keyword(s):  
Cell Death ◽  
Hearing Loss ◽  
Antioxidant Enzymes ◽  
Oral Administration ◽  
Hair Cell ◽  
Cell Survival ◽  
Sensory Cell ◽  
Auditory Function ◽  
Sensory Hair ◽  
Sensory Hair Cell

Noise induces oxidative stress in the cochlea followed by sensory cell death and hearing loss. The proof of principle that injections of antioxidant vitamins and Mg2+ prevent noise-induced hearing loss (NIHL) has been established. However, effectiveness of oral administration remains controversial and otoprotection mechanisms unclear. Using auditory evoked potentials, quantitative PCR and immunocytochemistry, we explored effects of oral administration of vitamins A, C, E and Mg2+ (ACEMg) on auditory function and sensory cell survival following NIHL in rats. Oral ACEMg reduced auditory thresholds shifts after NIHL. Improved auditory function correlated with increased survival of sensory outer hair cells. In parallel, oral ACEMg modulated the expression timeline of antioxidant enzymes in the cochlea after NIHL. There was increased expression of Glutathione peroxidase-1 and Catalase at 1 and 10 days, respectively. Also, pro-apoptotic Caspase-3 and Bax levels were diminished in ACEMg-treated rats, at 10 and 30 days, respectively, following noise overstimulation, whereas, at day 10 after noise exposure, the levels of anti-apoptotic Bcl-2, were significantly increased. Therefore, oral ACEMg improves auditory function by limiting sensory hair cell death in the auditory receptor following NIHL. Regulation of the expression of antioxidant enzymes and apoptosis-related proteins in cochlear structures is involved in such otoprotective mechanism.

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