TY - JOUR
T1 - Noise-induced hearing loss (NIHL) as a target of oxidative stress-mediated damage
T2 - Cochlear and cortical responses after an increase in antioxidant defense
AU - Fetoni, Anna Rita
AU - De Bartolo, Paola
AU - Eramo, Sara Letizia Maria
AU - Rolesi, Rolando
AU - Paciello, Fabiola
AU - Bergamini, Christian
AU - Fato, Romana
AU - Paludetti, Gaetano
AU - Petrosini, Laura
AU - Troiani, Diana
PY - 2013/2/27
Y1 - 2013/2/27
N2 - This study addresses the relationship between cochlear oxidative damage and auditory cortical injury in a rat model of repeated noise exposure. To test the effect of increased antioxidant defenses, a water-soluble coenzymeQ10 analog (Qter) was used.Weanalyzed auditory function, cochlear oxidative stress, morphological alterations in auditory cortices and cochlear structures, and levels of coenzymes Q9 and Q10 (CoQ9 and CoQ10, respectively) as indicators of endogenous antioxidant capability. We report three main results. First, hearing loss and damage in hair cells and spiral ganglion was determined by noise-induced oxidative stress. Second, the acoustic trauma altered dendritic morphology and decreased spine number of II-III and V-VI layer pyramidal neurons of auditory cortices. Third, the systemic administration of the water-soluble CoQ10 analog reduced oxidative-induced cochlear damage, hearing loss, and cortical dendritic injury. Furthermore, cochlear levels of CoQ9 and CoQ10 content increased. These findings indicate that antioxidant treatment restores auditory cortical neuronal morphology and hearing function by reducing the noise-induced redox imbalance in the cochlea and the deafferentation effects upstream the acoustic pathway.
AB - This study addresses the relationship between cochlear oxidative damage and auditory cortical injury in a rat model of repeated noise exposure. To test the effect of increased antioxidant defenses, a water-soluble coenzymeQ10 analog (Qter) was used.Weanalyzed auditory function, cochlear oxidative stress, morphological alterations in auditory cortices and cochlear structures, and levels of coenzymes Q9 and Q10 (CoQ9 and CoQ10, respectively) as indicators of endogenous antioxidant capability. We report three main results. First, hearing loss and damage in hair cells and spiral ganglion was determined by noise-induced oxidative stress. Second, the acoustic trauma altered dendritic morphology and decreased spine number of II-III and V-VI layer pyramidal neurons of auditory cortices. Third, the systemic administration of the water-soluble CoQ10 analog reduced oxidative-induced cochlear damage, hearing loss, and cortical dendritic injury. Furthermore, cochlear levels of CoQ9 and CoQ10 content increased. These findings indicate that antioxidant treatment restores auditory cortical neuronal morphology and hearing function by reducing the noise-induced redox imbalance in the cochlea and the deafferentation effects upstream the acoustic pathway.
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U2 - 10.1523/JNEUROSCI.2282-12.2013
DO - 10.1523/JNEUROSCI.2282-12.2013
M3 - Article
C2 - 23447610
AN - SCOPUS:84874627700
VL - 33
SP - 4011
EP - 4023
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 9
ER -