scholarly journals Reduced Formation of Oxidative Stress Biomarkers and Migration of Mononuclear Phagocytes in the Cochleae of Chinchilla after Antioxidant Treatment in Acute Acoustic Trauma

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Xiaoping Du ◽  
Chul-Hee Choi ◽  
Kejian Chen ◽  
Weihua Cheng ◽  
Robert A. Floyd ◽  
...  
Keyword(s):  
Hair Cell ◽  
Outer Hair Cell ◽  
Acoustic Trauma ◽  
Mononuclear Phagocytes ◽  
Auditory Brainstem Responses ◽  
Sensory Cells ◽  
Antioxidant Treatment ◽  
Cell Counts ◽  
And Migration ◽  
Acute Acoustic Trauma

Objective. Inhibition of inflammation and free radical formation in the cochlea may be involved in antioxidant treatment in acute acoustic trauma.Procedure. Chinchilla were exposed to 105 dB sound pressure level octave band noise for 6 hours. One group of chinchilla was treated with antioxidants after noise exposure. Auditory brainstem responses, outer hair cell counts, and immunohistochemical analyses of biomarkers in the cochlea were conducted.Results. The antioxidant treatment significantly reduced hearing threshold shifts, outer hair cell loss, numbers of CD45+cells, as well as 4-hydroxy-2-nonenal and nitrotyrosine formation in the cochlea.Conclusion. Antioxidant treatment may provide protection to sensory cells by inhibiting formation of reactive oxygen and nitrogen products and migration of mononuclear phagocytes in the cochlea. The present study provides further evidence of effectiveness of antioxidant treatment in reducing permanent hearing loss.

scholarly journals Hsp70/Bmi1-FoxO1-SOD Signaling Pathway Contributes to the Protective Effect of Sound Conditioning against Acute Acoustic Trauma in a Rat Model

2020 ◽  
Vol 2020 ◽  
pp. 1-22
Author(s):  
Guoxia Zhu ◽  
Yongxiang Wu ◽  
Yang Qiu ◽  
Keyong Tian ◽  
Wenjuan Mi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Rat Model ◽  
Molecular Mechanisms ◽  
Outer Hair Cell ◽  
Acoustic Trauma ◽  
Auditory Brainstem Responses ◽  
Ultrastructural Changes ◽  
Ganglion Neurons ◽  
Acute Acoustic Trauma

Sound conditioning (SC) is defined as “toughening” to lower levels of sound over time, which reduces a subsequent noise-induced threshold shift. Although the protective effect of SC in mammals is generally understood, the exact mechanisms involved have not yet been elucidated. To confirm the protective effect of SC against noise exposure (NE) and the stress-related signaling pathway of its rescue, we observed target molecule changes caused by SC of low frequency prior to NE as well as histology analysis in vivo and verified the suggested mechanisms in SGNs in vitro. Further, we investigated the potential role of Hsp70 and Bmi1 in SC by targeting SOD1 and SOD2 which are regulated by the FoxO1 signaling pathway based on mitochondrial function and reactive oxygen species (ROS) levels. Finally, we sought to identify the possible molecular mechanisms associated with the beneficial effects of SC against noise-induced trauma. Data from the rat model were evaluated by western blot, immunofluorescence, and RT-PCR. The results revealed that SC upregulated Hsp70, Bmi1, FoxO1, SOD1, and SOD2 expression in spiral ganglion neurons (SGNs). Moreover, the auditory brainstem responses (ABRs) and electron microscopy revealed that SC could protect against acute acoustic trauma (AAT) based on a significant reduction of hearing impairment and visible reduction in outer hair cell loss as well as ultrastructural changes in OHCs and SGNs. Collectively, these results suggested that the contribution of Bmi1 toward decreased sensitivity to noise-induced trauma following SC was triggered by Hsp70 induction and associated with enhancement of the antioxidant system and decreased mitochondrial superoxide accumulation. This contribution of Bmi1 was achieved by direct targeting of SOD1 and SOD2, which was regulated by FoxO1. Therefore, the Hsp70/Bmi1-FoxO1-SOD signaling pathway might contribute to the protective effect of SC against AAT in a rat model.

Effects of delayed and extended antioxidant treatment on acute acoustic trauma

2011 ◽  
Vol 45 (10) ◽  
pp. 1162-1172 ◽  
Author(s):  
Chul-Hee Choi ◽  
Kejian Chen ◽  
Xiaoping Du ◽  
Robert A. Floyd ◽  
Richard D. Kopke
Keyword(s):  
Acoustic Trauma ◽  
Antioxidant Treatment ◽  
Acute Acoustic Trauma

Effect of low-level laser treatment on cochlea hair-cell recovery after acute acoustic trauma

2012 ◽  
Vol 17 (6) ◽  
pp. 068002 ◽  
Author(s):  
Chung-Ku Rhee ◽  
Chan Woong Bahk ◽  
Se Hyung Kim ◽  
Jin-Chul Ahn ◽  
Jae Yun Jung ◽  
...  
Keyword(s):  
Hair Cell ◽  
Laser Treatment ◽  
Acoustic Trauma ◽  
Cell Recovery ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser ◽  
Acute Acoustic Trauma

scholarly journals Gene Delivery into the Inner Ear and Its Clinical Implications for Hearing and Balance

Molecules ◽  
2018 ◽  
Vol 23 (10) ◽  
pp. 2507 ◽  
Author(s):  
Sho Kanzaki
Keyword(s):  
Stem Cells ◽  
Hair Cell ◽  
Inner Ear ◽  
Viral Infections ◽  
Endolymphatic Hydrops ◽  
Topical Administration ◽  
Acoustic Trauma ◽  
Sensory Cells ◽  
Road Map ◽  
Cell Proliferation And Differentiation

The inner ear contains many types of cell, including sensory hair cells and neurons. If these cells are damaged, they do not regenerate. Inner ear disorders have various etiologies. Some are related to aging or are idiopathic, as in sudden deafness. Others occur due to acoustic trauma, exposure to ototoxic drugs, viral infections, immune responses, or endolymphatic hydrops (Meniere’s disease). For these disorders, inner ear regeneration therapy is expected to be a feasible alternative to cochlear implants for hearing recovery. Recently, the mechanisms underlying inner ear regeneration have been gradually clarified. Inner ear cell progenitors or stem cells have been identified. Factors necessary for regeneration have also been elucidated from the mechanism of hair cell generation. Inducing differentiation of endogenous stem cells or inner ear stem cell transplantation is expected. In this paper, we discuss recent approaches to hair cell proliferation and differentiation for inner ear regeneration. We discuss the future road map for clinical application. The therapies mentioned above require topical administration of transgenes or drug onto progenitors of sensory cells. Developing efficient and safe modes of administration is clinically important. In this regard, we also discuss our development of an inner ear endoscope to facilitate topical administration.

Round Window Application of D-Methionine Provides Complete Cisplatin Otoprotection

2002 ◽  
Vol 126 (6) ◽  
pp. 683-689 ◽  
Author(s):  
Kurtis D. Korver ◽  
Leonard P. Rybak ◽  
Craig Whitworth ◽  
Kathleen M. Campbell
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Outer Hair Cell ◽  
Round Window ◽  
Organ Of Corti ◽  
Cell Loss ◽  
Auditory Brainstem Responses ◽  
Round Window Membrane ◽  
Hair Cell Loss ◽  
Minute Amount

OBJECTIVE: Cisplatin is a widely used, very effective chemotherapeutic agent that can cause severe ototoxicity. In this study, D-methionine was tested as an otoprotectant via round window membrane (RWM) application in the chinchilla. METHODS: A minute amount of cisplatin alone, or D-methionine followed by cisplatin, was applied topically directly to the intact RWM of anesthetized adult chinchillas. Auditory brainstem responses were measured before and 1 week after topical round window application. Animals were killed, and the cochleas were examined. RESULTS: The ears pretreated with D-methionine were completely protected from hearing loss and hair cell loss in the organ of Corti compared with controls. The ears receiving cisplatin without D-methionine protection sustained nearly complete hearing loss with threshold shifts of >60 dB, with extensive outer hair cell loss throughout the organ of Corti but particularly in the basal turn. CONCLUSION: These results demonstrate that topical D-methionine provides excellent otoprotection against cisplatin-induced ototoxicity both electrophysiologically and structurally.

Total Energy and Critical Intensity Concepts in Noise Damage

1981 ◽  
Vol 90 (6) ◽  
pp. 584-590 ◽  
Author(s):  
W. Dixon Ward ◽  
Arndt J. Duvall ◽  
Peter A. Santi ◽  
Christopher W. Turner
Keyword(s):  
Hair Cell ◽  
Total Energy ◽  
Outer Hair Cell ◽  
Histological Study ◽  
Organ Of Corti ◽  
Acoustic Trauma ◽  
Energy Principle ◽  
Cell Destruction ◽  
Noise Damage ◽  
Critical Intensity

Groups of chinchillas were given a series of noise exposures of approximately equal energy ranging from 22 minutes at 120 dB SPL to 150 days at 82 dB. For all exposures involving levels of 112 dB or less, the same average permanent hearing losses (15–20 dB) and degree of outer hair cell destruction (8–10%) resulted, thus confirming the validity of the total energy principle for assessing the hazard associated with single continuous exposures at moderate levels. The 22-minute, 120-dB exposure, however, produced a 60-dB hearing loss and massive hair cell destruction (70–80%), indicating that some critical level had been exceeded, thus producing acoustic trauma. Further histological study suggests that the massive destruction is a result of breaks in the organ of Corti, produced by severe mechanical stress, that permit the mixture of endolymph with perilymph, thus creating a hostile environment for the hair cells.

Histological evaluation of cochlear hair cell damage from noise-induced hearing loss in chinchillas

1990 ◽  
Vol 48 (3) ◽  
pp. 332-333
Author(s):  
R.V. Harrison ◽  
R.J. Mount ◽  
P. White ◽  
N. Fukushima
Keyword(s):  
Hair Cell ◽  
Evoked Potential ◽  
Cell Damage ◽  
Acoustic Trauma ◽  
Histological Evaluation ◽  
Cell Integrity ◽  
Functional Changes ◽  
Cochlear Hair Cell ◽  
Left And Right ◽  
Contralateral Ear

In studies which attempt to define the influence of various factors on recovery of hair cell integrity after acoustic trauma, an experimental and a control ear which initially have equal degrees of damage are required. With in a group of animals receiving an identical level of acoustic trauma there is more symmetry between the ears of each individual, in respect to function, than between animals. Figure 1 illustrates this, left and right cochlear evoked potential (CAP) audiograms are shown for two chinchillas receiving identical trauma. For this reason the contralateral ear is used as control.To compliment such functional evaluations we have devised a scoring system, based on the condition of hair cell stereocilia as revealed by scanning electron microscopy, which permits total stereociliar damage to be expressed numerically. This quantification permits correlation of the degree of structural pathology with functional changes. In this paper wereport experiments to verify the symmetry of stereociliar integrity between two ears, both for normal (non-exposed) animals and chinchillas in which each ear has received identical noise trauma.

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