Impulse Noise-induced Hearing Loss Research Articles

Preloaded D-methionine protects from steady state and impulse noise-induced hearing loss and induces long-term cochlear and endogenous antioxidant effects.

ObjectiveDetermine effective preloading timepoints for D-methionine (D-met) otoprotection from steady state or impulse noise and impact on cochlear and serum antioxidant measures.DesignD-met started 2.0-, 2.5-, 3.0-, or 3.5- days before steady-state or impulse noise exposure with saline controls. Auditory brainstem response (ABRs) measured from 2 to 20 kHz at baseline and 21 days post-noise. Samples were then collected for serum (SOD, CAT, GR, GPx) and cochlear (GSH, GSSG) antioxidant levels.Study sampleTen Chinchillas per group.ResultsPreloading D-met significantly reduced ABR threshold shifts for both impulse and steady state noise exposures but with different optimal starting time points and with differences in antioxidant measures.For impulse noise exposure, the 2.0, 2.5, and 3.0 day preloading start provide significant threshold shift protection at all frequencies. Compared to the saline controls, serum GR for the 3.0 and 3.5 day preloading groups was significantly increased at 21 days with no significant increase in SOD, CAT or GPx for any impulse preloading time point. Cochlear GSH, GSSG, and GSH/GSSG ratio were not significantly different from saline controls at 21 days post noise exposure.For steady state noise exposure, significant threshold shift protection occurred at all frequencies for the 3.5, 3.0 and 2.5 day preloading start times but protection only occurred at 3 of the 6 test frequencies for the 2.0 day preloading start point. Compared to the saline controls, preloaded D-met steady-state noise groups demonstrated significantly higher serum SOD for the 2.5–3.5 day starting time points and GPx for the 2.5 day starting time but no significant increase in GR or CAT for any preloading time point. Compared to saline controls, D-met significantly increased cochlear GSH concentrations in the 2 and 2.5 day steady-state noise exposed groups but no significant differences in GSSG or the GSH/GSSG ratio were noted for any steady state noise-exposed group.ConclusionsThe optimal D-met preloading starting time window is earlier for steady state (3.5–2.5 days) than impulse noise (3.0–2.0). At 21 days post impulse noise, D-met increased serum GR for 2 preloading time points but not SOD, CAT, or GpX and not cochlear GSH, GSSG or the GSH/GSSG ratio. At 21 days post steady state noise D-met increased serum SOD and GPx at select preloading time points but not CAT or GR. However D-met did increase the cochlear GSH at select preloading time points but not GSSG or the GSH/GSSG ratio.

Pharmaceutical otoprotection strategies to prevent impulse noise-induced hearing loss.

One of the ongoing challenges for hearing researchers is successful protection of the ear from noise injury. For decades, the most effective methods have been based on modifying the acoustic properties of the noise, either by reducing noise output from various sources, interfering in the acoustic exposure path with environmental controls, or altering the noise dose for the individual with personal hearing protection devices. Because of the inefficiencies of some of the acoustic modification procedures, pharmaceutical otoprotection is targeted at making the cochlea less susceptible to injury. Short-duration, high-level impulse noises, typically caused by small-scale explosions, cause different sets of injuries in the ear than long-duration, low-variance noise exposures. Therefore, the expectation is that the ears exposed to impulse noise may need different pharmaceutical interventions, both in type of compounds used and the time course of administration of the compounds. The current review discusses four different classes of compounds that have been tested as impulse noise otoprotectants. In the process of describing those experiments, particular emphasis is placed on the acoustic properties of the impulses used, with the goal of providing context for evaluating the relevance of these different models to human impulse noise-induced hearing loss.

Little evidence for a chronotolerance effect for impulse noise exposure in the C57BL/6J mouse

Noise-induced hearing loss affects a large number of adults and children worldwide, and continues to be a major public health problem. The cochlea is an organ that maintains delicate metabolic homeostasis and precise mechanical architecture. Disruption of either can cause temporary or permanent injury. Impulse noises, which are short-duration, high-level bursts of sound caused by explosions, such as gunfire, can injure the cochlea through combinations of mechanical and metabolic injury. Susceptibility to the metabolic component of noise injury may vary with the circadian rhythm, a phenomenon known as chronotolerance. Chronotolerance to noise injury has been demonstrated for a one-hour noise exposure at a fixed level, but chronotolerance for impulse noise-induced hearing loss has never been studied. Forty-four mice were exposed to 500 short-duration clicks at 137 dB peSPL at one of four hours after light onset: 2, 8, 14, or 20. Auditory brainstem response threshold shifts were measured at 3, 7, and 21 days after the exposure to measure hearing loss, and post mortem outer hair cell counts were used to confirm cochlear injury. The testing revealed no significant differences between the four exposure times for hearing threshold shifts, but did detect a small, but statistically significant, difference in outer hair cell loss, in which the loss was greatest for the mice exposed two hours after light offset. Therefore, a weak chronotolerance effect for impulse noise was detected, though the functional significance of the effect is low. Further investigation is required to more fully understand the relationship between circadian rhythm and hearing loss from different types of noise exposure.

Radix astragali inhibits the down-regulation of connexin 26 in the stria vascularis of the guinea pig cochlea after acoustic trauma.

Connexin 26 (cx26) plays an important role in the intercellular signaling and is related to K(+) metabolism in stria vascularis (SV). Reactive oxygen species (ROS) are negative regulators of cx26, reducing intercellular coupling in cochlea. ROS plays an important role in acoustic trauma. Radix astragali is a natural antioxidant that decreases impulse noise-induced hearing loss through its ability to inhibit ROS. The purpose of this study was to investigate if radix astragali has the potential to reduce the change of cx26 in SV from impulse noise. Guinea pigs in the experimental group were administered radix astragali intraperitoneally. Auditory thresholds were assessed by sound-evoked auditory brainstem response (ABR) at click and tone bursts of 8, 16 and 32 kHz, 24 h before and 72 h after exposure to impulse noise. 4-Hydroxynonenal, cx26 and KCNQ1 were determined immunohistochemically in SV. SV was analyzed by transmission electron microscopy. Radix astragali significantly reduced the ABR deficits and the SV damage, and decreased the shifts of the expression of cx26 and KCNQ1 in the SV. These results suggest that the beneficial effect of radix astragali on impulse noise-induced hearing loss may be also due to its ability to reduce the change of cx26 in SV.

Development of a digital noise exposure system for research on noise induced hearing loss

Over thirty million Americans suffer from noise induced hearing loss (NIHL). Previous research demonstrated that different types of noises, even with equal sound energies, could produce different amounts of hearing loss. In this project, a novel digital noise exposure system has been developed for generating various noise signals (e.g. pure-tone, Gaussian, impulsive, and complex noise). The developed system can be used to study NIHL in animal models. The system could produce impulse noise with peak sound pressure level (SPL) up to 160 dB, which effectively mimics the noise generated by a military weapon (e.g., M-16 rifle). The preliminary results of in an animal study showed significant permanent threshold shift (PTS) produced by 90 shocks impulse noise with peak SPL = 155 dB generated by the system. In summary, the digital noise exposure system replicates environmental noise allowing researchers to study impulse noise induced hearing loss in a controlled situation.

Astragaloside IV inhibits apoptotic cell death in the guinea pig cochlea exposed to impulse noise

Conclusion: The results suggest that the beneficial effect of astragaloside IV on impulse noise-induced hearing loss may be due to its ability to inhibit reactive oxygen species (ROS) and prevent apoptosis. Objective: Astragaloside IV is the major active constituent of Astragalus membranaceus, which has been widely used for the treatment of diseases in China for its antioxidant properties. ROS and apoptosis are involved in damage induced by impulse noise trauma. We aimed to investigate if the beneficial effects of astragaloside IV on cochlea exposed to impulse noise are associated with the inhibition of ROS and the decrease in apoptosis. Methods: 4-Hydroxynonenal (HNE) was used as the marker of ROS. Active-caspase−3 (cas-3) served as a marker for apoptosis. 4HNE and cas-3 were determined immunohistochemically. Guinea pigs in the experimental group were administered astragaloside IV intragastrically. Auditory thresholds were assessed by sound-evoked auditory brainstem response (ABR) 72 h before and after exposure to impulse noise. Results: The results showed that astragaloside IV significantly reduced ABR deficits, and decreased the expression of ROS and cas-3.

Protection from impulse noise-induced hearing loss with novel Src-protein tyrosine kinase inhibitors

Apoptosis is a significant mechanism of cochlear hair cell loss from noise. Molecules that inhibit apoptotic intracellular signaling reduce cochlear damage and hearing loss from noise. The current study is an extension of a previous study of the protective value of Src-protein tyrosine kinase inhibitors against noise ( Harris et al., 2005). The current study tested three Src-inhibitors: the indole-based KX1-141, the biaryl-based KX2-329, and the ATP-competitive KX2-328. Each of the three drugs was delivered into the chinchillas’ cochleae by allowing the solutions to diffuse across the round window membrane thirty minutes prior to exposure to impulse noise. Hearing thresholds were measured using auditory evoked responses from electrodes in the inferior colliculi. Ears treated with KX2-329 showed significantly lower threshold shifts and outer hair cell losses than the control group. The cochleae treated with KX1-141 and KX2-328 did not show statistically significant protection from the impulse noise. The finding of protection with KX2-329 demonstrates that a biaryl-based Src inhibitor has protective capacity against noise-induced hearing loss that is as good as that demonstrated by KX1-004, a Src inhibitor drug that has been studied extensively as an otoprotectant against noise, and suggests that KX2-329 could be useful for protection against noise.

Astragaloside IV attenuates impulse noise-induced trauma in guinea pig

Conclusion. These results suggest that the beneficial effect of astragaloside IV on impulse noise-induced hearing loss may be due to its ability to inhibit inducible nitric oxide synthase (iNOS) and prevent the formation of reactive nitrogen species (RNS). Objective: Astragaloside IV is the major active constituent of Astragalus membranaceus, which has been widely used for the treatment of diseases in China due to its antioxidant properties. iNOS and RNS are involved in damage induced by impulse noise trauma. The purpose of the present study was to investigate if astragaloside IV has the potential to reduce cochlear damage from impulse noise. Methods: Guinea pigs in the experimental group were administered astragaloside IV intragastrically. Auditory thresholds were assessed by sound-evoked auditory brainstem response (ABR) at click and tone bursts of 8, 16 and 32 kHz, 72 h before and after exposure to impulse noise. iNOS and nitrotyrosine were determined immunohistochemically. Hair cell damage was analyzed by scanning electron microscopy. Results: Astragaloside IV significantly reduced ABR deficits, reduced hair cell damage, and decreased the expression of iNOS and RNS formation.

Leupeptin reduces impulse noise induced hearing loss

BackgroundExposure to continuous and impulse noise can induce a hearing loss. Leupeptin is an inhibitor of the calpains, a family of calcium-activated proteases which promote cell death. The objective of this study is to assess whether Leupeptin could reduce the hearing loss resulting from rifle impulse noise.MethodsA polyethelene tube was implanted into middle ear cavities of eight fat sand rats (16 ears). Following determination of auditory nerve brainstem evoked response (ABR) threshold in each ear, the animals were exposed to the noise of 10 M16 rifle shots. Immediately after the exposure, saline was then applied to one (control) ear and non-toxic concentrations of leupeptin determined in the first phase of the study were applied to the other ear, for four consecutive days.ResultsEight days after the exposure, the threshold shift (ABR) in the control ears was significantly greater (44 dB) than in the leupeptin ears (27 dB).ConclusionLeupeptin applied to the middle ear cavity can reduce the hearing loss resulting from exposure to impulse noise.

Low-dose, long-term caroverine administration attenuates impulse noise-induced hearing loss in the rat

Conclusion. Physiological and morphological assessments indicated that low-dose and long-term caroverine delivery might be a new approach to protect against impulse noise-induced hearing loss. Background. Although the exact mechanisms by which impulse noise causes hearing loss are still unclear, there is accumulating evidence that increased reactive oxygen species (ROS) production and excessive glutamate released from the inner hair cells lead to hair cell loss and consequently hearing loss. Caroverine is an antagonist of two glutamate receptors, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors in the inner ear, as well as an antioxidant. Materials and methods. In this study, caroverine was delivered subcutaneously using an osmotic pump. This kind of delivery has the advantage, via continuous, long-term and low dose drug administration, of avoiding systemic side effects. Results. It was shown that caroverine could significantly protect the cochlea against impulse noise trauma.

Prevention of impulse noise-induced hearing loss with antioxidants

ConclusionThese findings indicate a strong protective effect of ALCAR and NAC on impulse noise-induced cochlear damage, and suggest the feasibility of using clinically available antioxidant compounds to protect the ear from acute acoustic injury.ObjectiveReactive oxygen species have been shown to play a significant role in noise-induced hearing loss. In the current study, the protective effects of two antioxidants, acetyl-L-carnitine (ALCAR) and N-L-acetylcysteine (NAC), were investigated in a chinchilla model of hearing loss resulting from impulse noise. It was hypothesized that pre- and post-treatment with these antioxidants would ameliorate the effects of impulse noise compared to saline-treated controls.Material and methodsEighteen animals were randomly assigned to 1 of 3 groups and exposed to impulse noise at a level of 155 dB peak SPL for 150 repetitions. ALCAR or NAC were administered twice daily (b.i.d.) for 2 days and 1 h prior to and 1 h following noise exposure, and then b.i.d. for the following 2 days. For the control group, saline was injected at the same time points. Auditory brainstem responses (ABRs) were recorded. Cochlear surface preparations were made to obtain cytocochleograms.ResultsThree weeks after exposure, permanent threshold shifts for the experimental groups were significantly reduced to ≈10–30 dB less than that for the control group (p<0.01). Less hair cell loss was also observed in the ALCAR and NAC groups than in the control group.

Self-Reported Elevated Blood Pressure in Army Officers with Hearing Loss and Gunfire Noise Exposure

The association of noise-induced hearing loss from gunfire noise with the occurrence of elevated blood pressure was investigated with screening audiometric measurement results and a questionnaire in a randomly selected group of 699 army officers. After age correction, hearing was found to be deteriorated (i.e., more than 20 dB at all of the measured frequencies) in 352 (50.4%) subjects. Of the 699 officers, 535 (76.5%) reported normal and 164 (23.5%) reported elevated blood pressure. In 122 (17.5%), elevation was permanent and verified by a physician. The occurrence of elevated blood pressure showed a highly significant correlation with severity of hearing loss (chi-square = 25.4; p < 0.001), but not with exposure to gunfire noise. Self-reported hypertension seemed to be associated with severity of impulse noise-induced hearing loss, but not with the amount of gunfire noise exposure. Thus, the present study does not support the suggestion that there exists a simultaneous correlation between impulse noise exposure, noise-induced hearing loss, and self-reported elevated blood pressure.

Acoustic middle ear muscle reflex protection against magnetic coil impulse noise.

Electromagnetic stimulation (EMS) of the brain and the intracranial portion of the facial nerve has become a widely used clinical technique. The high intensity impulse noise acoustic artifact generated by some magnetic coils used in EMS has been shown to cause severe cochlear damage in experimental animals. This damage results in permanent threshold shifts throughout the auditory spectrum of the rabbit. As with other impulse and impact noise signals, the duration of the coil impulse noise is too short to be influenced by the normally protective acoustic middle ear muscle reflex. Artificially activating the acoustic reflex with a contralateral broad band noise during exposure to the intense coil artifact reduced the compound threshold shift (CTS) significantly, and the permanent threshold shifts (PTS) to near zero at each tone frequency and noise band tested. The results demonstrate the effectiveness of a suprathreshold sound in activating the acoustic middle ear muscle reflex and protecting against impulse noise-induced hearing loss caused by high frequency magnetic coil acoustic impulses.

Impulse Noise-Induced Hearing Loss in Drop Forge Operators and the Energy Concept

Impulse Noise-Induced Hearing Loss in Drop Forge Operators and the Energy Concept