ubiquinone and Hearing-Loss--Noise-Induced

Noise is a stress factor that causes auditory, psychological and physiological effects. The realization that sudden loud noises or chronic exposure to noise in social and working environments can cause hearing loss has led to increased interest in noise-induced hearing loss (NIHL). The best means of preventing primary damage is protection against noise. Since this protection is not always possible for various reasons, the use of pharmacological agents to prevent or treat NIHL should also be considered. The purpose of this study is to discuss current pharmacological protection and treatment options in the light of the literature, since no such extensive reviews have been performed to date, including agents used for protection against and treatment of NIHL. We reviewed both animal and clinical studies, and these are discussed separately for ease of comprehension. For each agent, first animal studies, then clinical studies, if available, are discussed. We also performed a two-step search of the literature. In the first step, we searched the terms "noise induced hearing loss", "treatment" and "protection" in Pubmed. Based on the results obtained, we identified the agents used for the treatment of and protection against NIHL. In the second step, we searched the names of the agents identified in the first step, together with the term "noise induced hearing loss," and reviewed the results.

Topics: Animals; Antioxidants; Calcium Channel Blockers; Dizocilpine Maleate; Excitatory Amino Acid Antagonists; Glucocorticoids; Hearing Loss, Noise-Induced; Humans; Magnesium; Methionine; Nerve Growth Factors; Ubiquinone; Vitamins

Experimental and human investigations have raised the level of concern about the potential ototoxicity of organic solvents and their interaction with noise. The main objective of this study was to characterize the effects of the combined noise and styrene exposure on hearing focusing on the mechanism of damage on the sensorineural cells and supporting cells of the organ of Corti and neurons of the ganglion of Corti. The impact of single and combined exposures on hearing was evaluated by auditory functional testing and histological analyses of cochlear specimens. The mechanism of damage was studied by analyzing superoxide anion and lipid peroxidation expression and by computational analyses of immunofluorescence data to evaluate and compare the oxidative stress pattern in outer hair cells versus the supporting epithelial cells of the organ of Corti. The oxidative stress hypothesis was further analyzed by evaluating the protective effect of a Coenzyme Q

Topics: Animals; Antioxidants; Hair Cells, Auditory, Inner; Hair Cells, Auditory, Outer; Hearing Loss, Noise-Induced; Labyrinth Supporting Cells; Lipid Peroxidation; Male; Noise; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Wistar; Styrene; Ubiquinone

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 coenzyme Q10 analog (Qter) was used. We analyzed 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.

Topics: Accessory Atrioventricular Bundle; Acoustic Stimulation; Aldehydes; Analysis of Variance; Animals; Antioxidants; Auditory Pathways; Brain Injuries; Cochlea; Disease Models, Animal; Ethidium; Evoked Potentials, Auditory, Brain Stem; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Male; Oxidative Stress; Rats; Rats, Wistar; Silver Staining; Ubiquinone; Visual Cortex

Data from animal studies show that antioxidants can compensate against noise-induced stress and sensory hair cell death. The aim of this study was to evaluate the otoprotection efficacy of various versions of orally administered Acuval 400 against noise damage in a rat animal model.. Fifty-five Sprague Dawley rats were divided into 4 groups: A) noise-exposed animals; B) animals exposed to noise and treated with the Acuval; C) animals exposed to noise and treated with a combination of Coenzyme Q10 and Acuval; D) animals treated only with Acuval and Coenzyme Q10 and with no exposure to noise. All solutions were administered orally 5 times: 24 and 2 hrs prior to noise exposure, and then daily for 3 days. The auditory function was assessed by measuring auditory brainstem responses (ABR) in the range from 2 to 32 kHz at times =1, 7, 14 and 21 days after noise exposure.. At low frequencies (click and 4 kHz) animals from both A and B groups showed significant threshold shifts in the majority of the tested frequencies and tested times. For the same frequencies, animals from group C presented threshold levels similar to those from group D. At frequencies ≥ 8 kHz the protective performance of the 2 Acuval groups is more clearly distinguished from the noise group A. At 32 kHz the 2 Acuval groups perform equally well in terms of otoprotection. Animals in Group D did not show any significant differences in the hearing threshold during the experiment.. The data of this study suggest that a solution containing Coenzyme Q10 and Acuval 400, administered orally, protects from noise-induced hearing loss.

Topics: Animals; Evoked Potentials, Auditory, Brain Stem; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Likelihood Functions; Models, Statistical; Protective Agents; Rats; Rats, Sprague-Dawley; Ubiquinone; Vitamins

The effectiveness of a coenzyme Q10 formulation, Q-ter, given via transtympanic injection is interesting for the future application of this minimally invasive procedure in the treatment of reactive oxygen species (ROS)-induced hearing loss.. We focused on antioxidant therapy in noise-induced hearing loss (NIHL). Our study was designed to evaluate the effectiveness of Q-ter for different schedules of drug administration to establish the best modality for treatment.. Rats were exposed to acoustic trauma (10 kHz at 120 dB for 60 min) and received Q-ter according to two modalities: systemic (Q-ter 100 mg/kg for 4 days 1 h before and 3 days post noise exposure) and transtympanic (Q-ter 20 and 40% concentration 1 h before noise exposure). Auditory brainstem response (ABR), immunohistochemical and morphological studies were performed.. Q-ter administration significantly decreased NIHL at day 21 from noise exposure. The improvement of auditory function by Q-ter was paralleled by a significant reduction in oxidative stress. The transtympanic and systemic routes of drug administration showed a similar degree of protection.

Topics: Animals; Antioxidants; Drug Evaluation, Preclinical; Evoked Potentials, Auditory, Brain Stem; Hair Cells, Auditory; Hearing Loss, Noise-Induced; In Situ Nick-End Labeling; Injections; Rats; Rats, Wistar; Reactive Oxygen Species; Ubiquinone

The mitochondrial respiratory chain is a powerful source of reactive oxygen species (ROS) also in noise induced hearing loss (NIHL) and anti-oxidants and free-radicals scavengers have been shown to attenuate the damage. Coenzyme Q(10) (CoQ(10)) or ubiquinone has a bioenergetic role as a component of the mithocondrial respiratory chain, it inhibits mitochondrial lipid peroxidation, inducing ATP production and it is involved in ROS removal and prevention of oxidative stress-induced apoptosis. However the therapeutic application of CoQ(10) is limited by the lack of solubility and poor bio- availability, therefore it is a challenge to improve its water solubility in order to ameliorate the efficacy in tissues and fluids. This study was conducted in a model of acoustic trauma in the guinea pig where the effectiveness of CoQ(10) was compared with a soluble formulation of CoQ(10) (multicomposite CoQ(10) Terclatrate, Q-ter) given intraperitoneally 1 h before and once daily for 3 days after pure tone noise exposure (6 kHz for 1 h at 120 dB SPL). Functional and morphological studies were carried out by measuring auditory brainstem responses, scanning electron microscopy for hair cell loss count, active caspase 3 staining and terminal deoxynucleotidyl transferase-mediated dUTP labelling assay in order to identify initial signs of apoptosis. Treatments decreased active caspase 3 expression and the number of apoptotic cells, but animals injected with Q-ter showed a greater degree of activity in preventing apoptosis and thus in improving hearing. These data confirm that solubility of Coenzyme Q(10) improves the ability of CoQ(10) in preventing oxidative injuries that result from mitochondrial dysfunction.

Topics: Acoustic Stimulation; Analysis of Variance; Animals; Apoptosis; Auditory Threshold; Caspase 3; Cell Count; Disease Models, Animal; Guinea Pigs; Hair Cells, Auditory, Outer; Hearing Loss, Noise-Induced; In Situ Nick-End Labeling; Microscopy, Confocal; Microscopy, Electron, Scanning; Solubility; Ubiquinone; Water

The results of this study indicate that coenzyme Q10 reduces cochlear oxidative stress induced by acoustic overstimulation.. We investigated the effects of coenzyme Q10 on noise-induced hearing loss in guinea pigs.. Animals received water-soluble coenzyme Q10 intraperitoneally 2 h before noise exposure. Seven days after noise exposure (130 dB sound pressure level for 3 h), the auditory brainstem response (ABR) threshold shift and cochlear hair cell damage were assessed.. We observed that the ABR threshold shift was significantly less in the coenzyme Q10 group than in the vehicle control group. In addition, the percentage of missing outer hair cells was lower in the coenzyme Q10 group than in the control group. Moreover, 2 days after administration of coenzyme Q10, increased antioxidative activity in the cochlea, as measured by analysis of hydroxy radical scavenging activity by electron spin resonance was observed.

Topics: Aldehydes; Animals; Antioxidants; Auditory Threshold; Electron Spin Resonance Spectroscopy; Evoked Potentials, Auditory, Brain Stem; Free Radical Scavengers; Guinea Pigs; Hair Cells, Auditory, Outer; Hearing Loss, Noise-Induced; Hydroxyl Radical; Immunohistochemistry; Male; Ubiquinone

Idebenone, a synthetic analogue of coenzyme Q, attenuates noise-induced hearing loss by virtue of its antioxidant properties. This study involves a guinea pig model of acoustic trauma where the effectiveness of idebenone is analyzed in comparison with Vitamin E (alpha-tocopherol) that exhibits a potent antioxidant activity in the inner ear. Idebenone and vitamin E were injected intraperitoneally 1 h before noise exposure and once daily for three days; functional and morphological studies were then carried out, respectively, by auditory brainstem responses evaluation, scanning electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling assay identification of missing and apoptotic cells was also performed. The results showed that the protective effects of idebenone and vitamin E were not additive implying that the two antioxidants may share competitive mechanisms.

Topics: Animals; Antioxidants; Benzoquinones; Drug Synergism; Electrophysiology; Guinea Pigs; Hearing; Hearing Loss, Noise-Induced; In Situ Nick-End Labeling; Microscopy, Electron, Scanning; Noise; Organ of Corti; Ubiquinone; Vitamin E

Idebenone is a synthetic analogue of coenzyme Q10 with antioxidant properties. The present study investigated the antioxidant activity of idebenone in the rescue of acoustic trauma. Noise-induced hearing loss was induced by exposing guinea pigs to a continuous pure tone and idebenone was injected intraperitoneally 1 h before noise exposure and once daily for 3 days. Guinea pigs treated with idebenone showed significantly smaller auditory threshold shifts than unprotected control animals. Missing and apoptotic cells were identified with scanning electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling assay. Protected animals presented a lesser extent of both apoptotic activation and hair cell loss in the organ of Corti. Our results suggest an antioxidant function of idebenone in protection from noise-induced hearing loss and provide a rationale for exploring therapeutic strategies in humans.

Topics: Acoustic Stimulation; Analysis of Variance; Animals; Antioxidants; Apoptosis; Auditory Threshold; Benzoquinones; Dose-Response Relationship, Radiation; Guinea Pigs; Hearing Loss, Noise-Induced; In Situ Nick-End Labeling; Microscopy, Electron, Scanning; Time Factors; Ubiquinone

Observations have been made on the effect of intermittent intense sound stimuli, using the CM as an index. Experiments were conducted regarding the effectiveness of the drug CoQ10 in ameliorating the acoustic injury due to this traumatization. The CM was measured by the differential electrode method from the basal turn of the cochlea. The individual differences between animals were monitored using intensity functions. Pure tones at a frequency of 4 kHz were used both for the traumatizing signal and the CM generating signal. Acoustic traumatizing signals lasted 1 min with a 5 min silent interval, and were repeated 10 times. Both the chronic depression and the transient depression of CM were measured after each traumatization. In control animals, the chronic depression progressed in an exponential manner and the transient depression was constant after each stimulation. In CoQ10 treated animals, the chronic depression was milder than that in the control animals. The transient depression was equivalent in the two groups. The effectiveness of CoQ10 on the acoustic injury was discussed on the basis of the results obtained with the present experiment.

Topics: Acoustic Stimulation; Animals; Cochlear Microphonic Potentials; Disease Models, Animal; Evoked Potentials, Auditory; Guinea Pigs; Hearing Loss, Noise-Induced; Ubiquinone