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 ◽  
...  

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.

Author(s):  
Juan C Alvarado ◽  
Veronica Fuentes-Santamaría ◽  
Pedro Melgar-Rojas ◽  
Maria C Gabaldon-Ull ◽  
Jose J Cabanes-Sanchis ◽  
...  

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.


PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e55359 ◽  
Author(s):  
Phillip M. Uribe ◽  
Melissa A. Mueller ◽  
Julia S. Gleichman ◽  
Matthew D. Kramer ◽  
Qi Wang ◽  
...  

Author(s):  
Jerry D. Monroe ◽  
Gopinath Rajadinakaran ◽  
Michael E. Smith

2021 ◽  
Author(s):  
Pei Zhuang ◽  
Suiching Phung ◽  
Athanasia Warnecke ◽  
Alexandra Arambula ◽  
Madeleine St. Peter ◽  
...  

AbstractEvaluation of hearing loss patients using clinical audiometry has been unable to give a definitive cellular or molecular diagnosis, hampering the development of treatments of sensorineural hearing loss. However, biopsy of inner ear tissue without losing residual hearing function for pathologic diagnosis is extremely challenging. In a clinical setting, perilymph can be accessed, so alternative methods for molecular characterization of the inner ear may be developed. Recent approaches to improving inner ear diagnostics have been focusing on the evaluation of the proteomic or miRNA profiles of perilymph. Inspired by recent characterization and classification of many neurodegenerative diseases using exosomes which not only are produced in locally in diseased tissue but are transported beyond the blood brain barrier, we demonstrate the isolation of human inner ear specific exosomes using a novel ultrasensitive immunomagnetic nano pom-poms capture-release approach. Using perilymph samples harvested from surgical procedures, we were able to isolate exosomes from sensorineural hearing loss patients in only 2-5 μL of perilymph. By isolating sensory hair cell derived exosomes through their expression level of myosin VII, we for the first time sample material from hair cells in the living human inner ear. This work sets up the first demonstration of immunomagnetic capture-release nano pom-pom isolated exosomes for liquid biopsy diagnosis of sensorineural hearing loss. With the ability to isolate exosomes derived from different cell types for molecular characterization, this method also can be developed for analyzing exosomal biomarkers from more accessible patient tissue fluids such as plasma.


Author(s):  
Michael E. Smith ◽  
Andrew K. Groves ◽  
Allison B. Coffin

1977 ◽  
Vol 55 (1) ◽  
pp. 223-230 ◽  
Author(s):  
F. Ramprashad ◽  
K. Ronald

Surface preparations of the organ of Corti of four harp seals were used to study the effect of prolonged ingestion of methyl mercury on the sensory cell population.A low level of damage to the sensory hair cells occurred throughout the length of the cochlea. Damage was confined to the three outer rows of sensory hair cells especially the third outermost row. At each location along the length of the cochlea, sensory hair cell damage in the seals on a daily dose of 25.0 mg/kg of methyl mercury exceeded the damage to the cochlea of the seals fed on a daily dose of 0.25 mg/kg of methyl mercury. Greatest damage in all the mercury-treated seals occurred in the middle coil of the cochlea. Seals on the higher mercury diet showed a 20–24% sensory cell damage at the upper middle coil, about 19–26 mm from the base, whereas only 4–5% damage was found within same region in the cochlea of the seals on the lower mercury diet.This lack of specificity and low level of damage to the sensory hair cells seems characteristic of mercury and is a direct contrast to other known ototoxic agents.


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