Protective Effect of Ginsenoside Rd on Military Aviation Noise-Induced Cochlear Hair Cell Damage

2021 ◽  
Author(s):  
Xuemin Chen ◽  
Yu-hui LIU ◽  
Shuai-fei JI ◽  
Xin-miao XUE ◽  
Peng LIU ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hair Cell ◽  
Signaling Pathway ◽  
Cell Damage ◽  
Outer Hair Cells ◽  
Ginsenoside Rd ◽  
Cochlear Hair Cell ◽  
Aviation Noise ◽  
Military Aviation ◽  
Hair Cell Damage

Abstract Background Soldiers are often exposed to high-intensity noise produced by military weapons and equipment during activities, and the incidence of noise-induced hearing loss (NIHL) in many arms is high. Oxidative stress has a significant role in the pathogenesis of NIHL, and research has confirmed that ginsenoside Rd (GSRd) suppresses oxidative stress. Therefore, we hypothesized that GSRd may attenuate NIHL and cochlear hair cell loss, induced by military aviation noise stimulation, through the Sirtuin1/proliferator-activated receptor-gamma coactivator 1α (SIRT1/PGC-1α) signaling pathway.Methods Forty-eight male guinea pigs were randomly divided into four groups: control, noise stimulation, GSRd, and glycerol. The experimental groups received military helicopter noise stimulation at 115 dB (A) for 4 h daily for five consecutive days. Hair cell damage was evaluated by using inner ear basilar membrane preparation and scanning electron microscopy. Terminal dUTP nick end labeling and immunofluorescence staining were conducted. Changes in the SIRT1/PGC-1α signaling pathway and other apoptosis-related markers in the cochleae, as well as oxidative stress parameters were used as readouts.Results Loss of outer hair cells, more disordered cilia, prominent apoptosis, and elevated free radical levels were observed in the experimental groups. GSRd treatment markedly improved morphological changes and apoptosis through decreasing Bcl-2 associated X protein (Bax) expression and increasing Bcl-2 expression. In addition, GSRd upregulated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels, decreased malondialdehyde (MDA) levels, and enhanced the activity of SIRT1 and PGC-1α messenger ribonucleic acid and protein expression.Conclusion GSRd can improve structural and functional damage to the cochleae caused by noise. The underlying mechanisms may be associated with the SIRT1/PGC-1α signaling pathway.

Early Evidence of Cochlear Damage in a Large Sample of Percussionists

2005 ◽  
Vol 20 (3) ◽  
pp. 135-139
Author(s):  
Jodee A Pride ◽  
David R Cunningham
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Otoacoustic Emissions ◽  
Outer Hair Cell ◽  
Cell Damage ◽  
Normal Hearing ◽  
Outer Hair Cells ◽  
Sensory Loss ◽  
Distortion Product ◽  
Hair Cell Damage

Percussionists can be exposed to intermittent sound stimuli that exceed 145 dB SPL, although damage may occur to the outer hair cells at levels of 120 dB SPL. The present study measured distortion-product otoacoustic emissions (DPOAEs) in a group of 86 normal-hearing percussionists and 39 normal-hearing nonpercussionists. Results indicate that normal-hearing percussionists have lower DPOAE amplitudes than normal-hearing nonpercussionists. DPOAE amplitudes were significantly lower at 6000 Hz in both the left and right ears for percussionists. Percussionists also more frequently had absent DPOAEs, with the greatest differences occurring at 6000 Hz (absent DPOAEs in 25% of percussionists vs 10% of nonpercussionists). When all frequencies are considered as a group, 33% of the percussionists had an absent DPOAE in either ear at some frequency, compared to only 23% of the nonpercussionists. Otoacoustic emissions are more sensitive to outer hair cell damage than pure-tone threshold measurements and can serve as an important measurement of sensory loss (i.e., outer hair cell damage) in musicians before the person perceives the hearing loss. DPOAE monitoring for musicians, along with appropriate education and intervention, might help prevent or minimize music-induced hearing loss.

Ultrastructural Changes in the Cochlea of the Guinea Pig after Fast Neutron Irradiation

1994 ◽  
Vol 110 (4) ◽  
pp. 419-427 ◽  
Author(s):  
Ilsa Schwartz ◽  
Chong-Sun Kim ◽  
See-Ok Shin
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Hair Cell ◽  
Neutron Irradiation ◽  
Hair Cells ◽  
Cell Damage ◽  
Outer Hair Cells ◽  
Transmission Electron ◽  
Fast Neutron Irradiation ◽  
Hair Cell Damage

Guinea pigs were irradiated with fast neutrons. After a single dose of 2, 6, 10, or 15 Gy was applied, scanning and transmission electron microscopy of the temporal bone was performed to assess the effect of fast neutron irradiation on the cochlea. Outer hair cell damage appeared with neutron irradiation of more than 10 Gy, and Inner hair cell damage with neutron Irradiation of more than 15 Gy. Outer hair cells were more severely damaged than Inner hair cells. No statistically significant differences were found in damage of basal, middle, and apical turns. The second and third rows of outer hair cells were more severely damaged than the first row of outer hair cells. The most significant findings in transmission electron microscopy were clumping of chromatin and extension of the heterochromatin in the nuclei of hair cells. The cytoplasmic changes were sequestration of cytoplasm, various changes of mitochondria, formation of vacuoles, and irregularly arranged stereocilia. The morphologic change in stria vascularis was intercellular and perivascular fluid accumulation. It appeared to be a reversible process.

Cochlear Hair‐Cell Damage in Guinea Pigs after Exposure to Impulse Noise

1969 ◽  
Vol 46 (4B) ◽  
pp. 947-951 ◽  
Author(s):  
Lynn B. Poche ◽  
Charles W. Stockwell ◽  
Harlow W. Ades
Keyword(s):  
Hair Cell ◽  
Guinea Pigs ◽  
Impulse Noise ◽  
Cell Damage ◽  
Cochlear Hair Cell ◽  
Hair Cell Damage

scholarly journals Unmyelinated type II afferent neurons report cochlear damage

2015 ◽  
Vol 112 (47) ◽  
pp. 14723-14727 ◽  
Author(s):  
Chang Liu ◽  
Elisabeth Glowatzki ◽  
Paul Albert Fuchs
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Outer Hair Cell ◽  
Cell Damage ◽  
Large Diameter ◽  
Outer Hair Cells ◽  
Type I ◽  
Type Ii ◽  
Inner Hair Cell ◽  
Hair Cell Damage

In the mammalian cochlea, acoustic information is carried to the brain by the predominant (95%) large-diameter, myelinated type I afferents, each of which is postsynaptic to a single inner hair cell. The remaining thin, unmyelinated type II afferents extend hundreds of microns along the cochlear duct to contact many outer hair cells. Despite this extensive arbor, type II afferents are weakly activated by outer hair cell transmitter release and are insensitive to sound. Intriguingly, type II afferents remain intact in damaged regions of the cochlea. Here, we show that type II afferents are activated when outer hair cells are damaged. This response depends on both ionotropic (P2X) and metabotropic (P2Y) purinergic receptors, binding ATP released from nearby supporting cells in response to hair cell damage. Selective activation of P2Y receptors increased type II afferent excitability by the closure of KCNQ-type potassium channels, a potential mechanism for the painful hypersensitivity (that we term “noxacusis” to distinguish from hyperacusis without pain) that can accompany hearing loss. Exposure to the KCNQ channel activator retigabine suppressed the type II fiber’s response to hair cell damage. Type II afferents may be the cochlea’s nociceptors, prompting avoidance of further damage to the irreparable inner ear.

Roles of Bak and Sirt3 in Paraquat-Induced Cochlear Hair Cell Damage

2021 ◽  
Author(s):  
Dalian Ding ◽  
Tomas Prolla ◽  
Shinichi Someya ◽  
Senthilvelan Manohar ◽  
Richard Salvi
Keyword(s):  
Hair Cell ◽  
Cell Damage ◽  
Cochlear Hair Cell ◽  
Hair Cell Damage

scholarly journals Trehalose protects against cisplatin-induced cochlear hair cell damage by activating TFEB-mediated autophagy

2021 ◽  
pp. 114904
Author(s):  
Zhuangzhuang Li ◽  
Qingxiu Yao ◽  
Yuxin Tian ◽  
Yumeng Jiang ◽  
Maoxiang Xu ◽  
...  
Keyword(s):  
Hair Cell ◽  
Cell Damage ◽  
Cochlear Hair Cell ◽  
Hair Cell Damage

III. Comparative Quantitative Analysis

1980 ◽  
Vol 89 (6_suppl3) ◽  
pp. 17-24 ◽  
Author(s):  
Irwin A. Ginsberg ◽  
Michael D. Rudnick ◽  
Pamela S. Huber
Keyword(s):  
Quantitative Analysis ◽  
Hair Cell ◽  
Cell Damage ◽  
Drug Effects ◽  
Systemic Administration ◽  
Aminoglycoside Antibiotics ◽  
Cochlear Hair Cell ◽  
Hair Cell Damage ◽  
Degree Of Damage ◽  
Topographic Pattern

Hypotheses to explain the selective ototoxicity of aminoglycoside antibiotics may be grouped into two categories: 1) a partition effect and 2) innate hair cell selectivity. The results of this study give evidence that, in fact, both mechanisms may interplay. This conclusion is induced from the observations that following the transtympanic administration of streptomycin, dihydrostreptomycin and neomycin: 1) All three drugs elicited nearly the same topographic pattern and degree of damage in the vestibular compartment. 2) All three drugs elicited nearly the same topographic pattern but widely different degrees of damage in the cochlear compartment (neomycin > > streptomycin > dihydrostreptomycin). 3) Neomycin caused the same devastating cochlear hair cell damage as reported for its systemic administration. 4) Dihydrostreptomycin was significantly more vestibulotoxic than cochleotoxic, and streptomycin was both significantly more cochleotoxic than vestibulotoxic and significantly more cochleotoxic than was dihydrostreptomycin. The latter observations are discussed with regard to contrasts with the literature reporting the drug effects following systemic administration.

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