scholarly journals Hyperbaric Oxygen Treatment Ameliorates Hearing Loss and Auditory Cortex Injury in Noise Exposed Mice by Repressing Local Ceramide Accumulation

2019 ◽  
Vol 20 (19) ◽  
pp. 4675 ◽  
Author(s):  
Su ◽  
Guo ◽  
Cheng ◽  
Zhang ◽  
Xie ◽  
...  

Noise-induced hearing loss (NIHL) relates closely to auditory cortex (AC) injury, so countermeasures aiming at the AC recovery would be of benefit. In this work, the effect of hyperbaric oxygen treatment on NIHL was elucidated, which was imposed on mice before (HBOP), during (HBOD) or after (HBOA) noise exposure. Morphology of neurons was assayed by hematoxylin-eosin or Nissl staining. Ceramide (Cer) level was measured through immunohistochemistry analysis. Apoptotic neurons were counted using transferase-mediated dUTP nick end labeling (TUNEL) staining. We demonstrated that the intense, broad band noise raised the threshold of auditory brainstem response, evoked neuronal degeneration or apoptosis and triggered the Cer accumulation in AC, all of which were restored significantly by HBOP, but not HBOD or HBOA. Cer over-generation reversed the advantages of HBOP significantly, while its curtailment recapitulated the effect. Next, noise exposure raised the superoxide or malondialdehyde (MDA) production which was blocked by HBOP or Cer repression. Oxidative control not only attenuated the hearing loss or neurodegeneration but, in turn, reduced the Cer formation significantly. In summary, mutual regulation between Cer and oxidative stress underlies the HBOP’s curative effect on hearing loss and neuronal damage in noise-exposed mice.

ORL ◽  
2008 ◽  
Vol 70 (3) ◽  
pp. 210-213 ◽  
Author(s):  
Markus C. Frantz ◽  
Bertram F. Pontz ◽  
Wolfgang Arnold

2020 ◽  
Vol 47 (9) ◽  
pp. 1564-1574
Author(s):  
Xingxing Meng ◽  
Xi Zhang ◽  
Yuting Su ◽  
Zhenghui Gu ◽  
Xiaoping Xie ◽  
...  

2020 ◽  
pp. 261-265
Author(s):  
Jonathan W. Brügger ◽  
Glenn A. Rauscher ◽  
John P. Florian ◽  

Hyperoxic myopia is a phenomenon reported in individuals who have prolonged exposure to an increased partial pressure of oxygen (PO2) and subsequently have a myopic (nearsighted) change in their vision. To date, there are numerous accounts of hyperoxic myopia in dry hyperbaric oxygen treatment patients; however, there have been only three confirmed cases reported in wet divers. This case series adds four confirmed cases of hyperoxic myopia in wet divers using 1.35 atmospheres (ATM) PO2 at the Navy Experimental Diving Unit (NEDU). The four divers involved were the first author’s patients at NEDU. Conditions for two divers were confirmed via record review, whereas the other two divers were diagnosed by the first author. All subjects were interviewed to correlate subjective data with objective findings. Each subject completed five consecutive six-hour hyperoxic (PO2 of 1.35 ATM) dives with 18-hour surface intervals. Each individual was within the U. S. Navy Dive Manual’s standards for general health. Visual acuity was measured prior to diving. Within three to four days after diving, the individuals reported blurry vision with an associated myopic refraction shift. Each diver had spontaneous resolution of his myopia over the next two to three weeks, with no significant residual symptoms. The divers in this case series were exposed to an increased PO2 (1.35 ATM for 30 hours over five days), a lesser exposure than that in other reports of hyperoxic myopia in wet divers diagnosed with hyperoxic myopia (1.3-1.6 ATM for 45-85 hours in 12-18 days). Furthermore, this pulse of exposure was more concentrated than typically seen with traditional hyperbaric oxygen therapy. Hyperoxic myopia continues to be a risk for those conducting intensive diving with a PO2 between 1.3-1.6 ATM. Additional investigation is warranted to better define risk factors and PO2 limits regarding ocular oxygen toxicity.


2017 ◽  
Vol 44 (6) ◽  
pp. 497-508 ◽  
Author(s):  
Enrico Camporesi ◽  
◽  
Giuliano Vezzani ◽  
Vincenzo Zanon ◽  
Daniele Manelli ◽  
...  

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 443
Author(s):  
Hyunjun Woo ◽  
Min-Kyung Kim ◽  
Sohyeon Park ◽  
Seung-Hee Han ◽  
Hyeon-Cheol Shin ◽  
...  

One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga Ecklonia cava, are potent antioxidant agents. In this study, we investigated the effect of PFF-A and dieckol on the consequences of noise exposure in mice. In 1,1-diphenyl-2-picrylhydrazyl assay, dieckol and PFF-A both showed significant radical-scavenging activity. The mice were exposed to 115 dB SPL of noise one single time for 2 h. Auditory brainstem response(ABR) threshold shifts 4 h after 4 kHz noise exposure in mice that received dieckol were significantly lower than those in the saline with noise group. The high-PFF-A group showed a lower threshold shift at click and 16 kHz 1 day after noise exposure than the control group. The high-PFF-A group also showed higher hair cell survival than in the control at 3 days after exposure in the apical turn. These results suggest that noise-induced hair cell damage in cochlear and the ABR threshold shift can be alleviated by dieckol and PFF-A in the mouse. Derivatives of these compounds may be applied to individuals who are inevitably exposed to noise, contributing to the prevention of noise-induced hearing loss with a low probability of adverse effects.


2013 ◽  
Vol 34 (4) ◽  
pp. e237-e243 ◽  
Author(s):  
Caferi Tayyar Selçuk ◽  
Burhan Özalp ◽  
Mustafa Durgun ◽  
Alicem Tekin ◽  
Mehmet Fatih Akkoç ◽  
...  

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