salicylates and Hearing-Loss--Noise-Induced

Topics: Animals; Animals, Newborn; Female; Gentamicins; Guinea Pigs; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Hearing Loss, Sensorineural; Magnesium; Magnesium Deficiency; Pregnancy; Rats; Salicylates; Salicylic Acid

The following is a review of the literature on interaction of noise and other agents, both ototraumatic and nonototraumatic. A short description of the anatomical effects of exposure to intense sound previews the interaction literature. The effects of exposure to combinations of continuous and impulse noise are discussed. This is followed by a review of data on interactions of noise and ototoxic drugs and noise and whole-body vibration, including discussion of putative mechanisms of synergism. In addition, preliminary results of noise-cisplatinum interaction are presented which suggest that if cisplatinum is presented during noise exposure in dose schedules simulating human chemotherapy schedules, hearing threshold shifts and histological damage is much greater than that caused by either agent in isolation. The clinical relevance of the interactions is discussed, along with potential synergistic interactions not yet investigated.

Topics: Aminoglycosides; Animals; Anti-Bacterial Agents; Cisplatin; Cochlea; Diuretics; Hearing Loss, Noise-Induced; Humans; Noise; Salicylates; Vibration

Salicylate intoxication is a cause of tinnitus and comorbidly associated with anxiety in humans. In a previous work, we showed that salicylate induces anxiety-like behavior and hippocampal type 2 theta oscillations (theta2) in mice. Here we investigate if the anxiogenic effect of salicylate is dependent on age and previous tinnitus experience. We also tested whether a single dose of DMT can prevent this effect. Using microwire electrode arrays, we recorded local field potential in young (4-5- month-old) and old (11-13-month-old) mice to study the electrophysiological effect of tinnitus in the ventral hippocampus (vHipp) and medial prefrontal cortex (mPFC) in an open field arena and elevated plus maze 1h after salicylate (300mg/kg) injection. We found that anxiety-like behavior and increase in theta2 oscillations (4-6 Hz), following salicylate pre-treatment, only occurs in young (normal hearing) mice. We also show that theta2 and slow gamma oscillations increase in the vHipp and mPFC in a complementary manner during anxiety tests in the presence of salicylate. Finally, we show that pre-treating mice with a single dose of the hallucinogenic 5-MeO-DMT prevents anxiety-like behavior and the increase in theta2 and slow gamma oscillations after salicylate injection in normal hearing young mice. This work further support the hypothesis that anxiety-like behavior after salicylate injection is triggered by tinnitus and require normal hearing. Moreover, our results show that hallucinogenic compounds can be effective in treating tinnitus-related anxiety.

Topics: Aging; Animals; Anxiety; Behavior, Animal; Electroencephalography; Evoked Potentials, Auditory, Brain Stem; Hallucinogens; Hearing Loss, Noise-Induced; Hippocampus; Male; Methoxydimethyltryptamines; Mice; Mice, Inbred C57BL; Microelectrodes; Motor Activity; Prefrontal Cortex; Salicylates; Tinnitus

Tinnitus, also called phantom auditory perception, is a major health problem in western countries. As such, a significant amount of effort has been devoted to understanding its mechanisms, including studies in animals wherein a supposed "tinnitus state" can be induced. Here, we studied on the same awake animals the effects of a high-dose of salicylate and of an acoustic trauma both at levels known to induce tinnitus. Recordings of cortical activity (local field potentials) from chronically implanted electrodes in the same animals under each condition allowed direct comparison of the effects of salicylate and trauma (noise trauma was carried out several days after full recovery from salicylate administration). Salicylate induced a systematic and reversible increase in amplitude of cortical responses evoked by tone bursts over a wide range of frequencies and intensities. The effects of noise trauma, though much more variable than those of salicylate, resulted in both increases and decreases in the amplitude of cortical responses. These alterations of cortical response amplitudes likely reflect associated hypoacusis and hyperacusis. The effects of salicylate administration and noise trauma on spontaneous activity were also studied. Fourier analysis did not reveal any increase in power within any given frequency band; rather, both treatments induced a decrease of power spectrum over a relatively broad frequency band (approximately 10-30 Hz). Entropy rate of spontaneous activity, a measure of complexity (temporal correlations), was found to decrease after salicylate but not after acoustic trauma. The present data on evoked potentials confirm salicylate effects at the cortical level and partially extend such effects to acoustic trauma. While the present study showed that both salicylate and noise trauma induced some changes of spontaneous activity in auditory cortex, none of these changes are interpretable in terms of potential neural correlate of tinnitus.

Topics: Acoustic Stimulation; Action Potentials; Animals; Auditory Cortex; Auditory Pathways; Disease Models, Animal; Dose-Response Relationship, Drug; Ear, Inner; Evoked Potentials, Auditory; Guinea Pigs; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Hyperacusis; Neurotoxins; Noise; Salicylates; Tinnitus; Wakefulness

The effects of a combination of two antioxidant compounds were studied in a chinchilla model of noise-induced hearing loss. After obtaining baseline hearing thresholds using inferior colliculus evoked potentials, chinchillas were exposed for 6 h to octave band noise centered at 4 kHz (105 dB SPL). Post-noise thresholds were obtained 1 h after the noise exposure, and then animals received either saline or salicylate and N-L-acetylcysteine combination. Another group received antioxidant treatment 1 h prior to noise. Hearing was tested at 1, 2 and 3 weeks post-noise. Subsequently, the cochleae were harvested, and cytocochleograms were prepared. There was a 20-40 dB SPL threshold shift at 3 weeks for tested controls. Permanent threshold shifts (PTS) were significantly reduced (P<0.05) to approximately 10 dB for the pre-treatment group at week 3. The PTS for the post-treatment group at week 3 was similar to the pre-treatment group at 1 and 2 kHz (0-10 dB) but was intermediate between the control and pre-treatment groups at 4 and 8 kHz (23 dB). Animals pre-treated with antioxidant had a significant reduction in hair cell loss but those post-treated with antioxidant had no protection from hair cell loss. These findings demonstrate the feasibility of reduction of noise-induced hearing loss using clinically available antioxidant compounds.

Topics: Acetylcysteine; Animals; Audiometry; Auditory Threshold; Cell Count; Chinchilla; Drug Combinations; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Salicylates

To investigate the effects of salicylate on noise-induced hearing loss (NIHL) in guinea pigs.. The animals were allocated into four groups (salicylate + noise, saline + noise, noise only and salicylate only) and were exposed to a 4 kHz octave band noise at 105 dB SPL for 2 hours for 5 consecutive days. Dynamic changes of ABR thresholds evoked by clicks were monitored. After physiological examination, the cochleae were processed for the morphological examination by light microscopy.. Mean thresholds of ABRs in the experimental group obtained on 5th day of the noise exposure was positively lower than the control groups (P < 0.05). The similar trends of ABR changes were found during other exposure days and after exposure, but the differences were not statistically significant. In the experimental group, there were 37.00 +/- 8.89 hair cell loses as assessed by nucleus staining, and 3.20 +/- 1.07 hair cells with nuclear deformation. The noise group had 74.11 +/- 10.28 hair cell loses and 10.43 +/- 9.71 hair cells with nuclear deformation, whereas the saline group had 63.60 +/- 7.97 hair cell loses and 20.80 +/- 15.48 hair cells with nuclear deformation. The difference between two groups was significant (P < 0.05).. The results suggest that administration of salicylate facilitates the recovery of cochlear hearing and reduces damage to hair cells after noise exposure.

Topics: Animals; Cochlea; Evoked Potentials, Auditory, Brain Stem; Guinea Pigs; Hair Cells, Auditory; Hearing Loss, Noise-Induced; Salicylates

Mongolian gerbils were exposed to either alpha-ketoglutarate, salicylate, or an 8-kHz pure tone. Cochlear microphonic (CM) was recorded from the round window in response to 68 and 88 dB SPL Gaussian noise. A nonlinear systems identification technique provided the frequency-domain parameters of a third-order polynomial model characterizing cochlear mechano-electric transduction (MET). A series of physiologic indices were derived from further exploration of the model. Exposure to the 8-kHz pure tone and round window application of salicylate resulted in different changes in the polynomial parameters and physiologic indices even though the threshold shifts were similar. A general reduction of CM magnitude was found after the tone exposure, and an increase at low-mid frequencies was demonstrated in the salicylate group especially at the lower signal level. The slope of the MET curve was reduced by the acoustic overstimulation. The root or the operating point of the MET was shifted in opposite directions after the two treatments. Sound-pressure levels that saturate MET expanded in the tone exposure group and narrowed in the salicylate group. The signal level also had effects on these indices.

Topics: Animals; Auditory Fatigue; Cochlea; Cochlear Microphonic Potentials; Gerbillinae; Hearing Loss, High-Frequency; Hearing Loss, Noise-Induced; Ketoglutaric Acids; Radiation-Protective Agents; Salicylates

A detailed analysis of risk factors for the development of sensorineural hearing loss (SNHL) was carried out in 199 forest workers. The hearing threshold of both ears at 4000 Hz was measured, and the effect of age, exposure to noise, blood pressure, presence of vibration induced white finger (VWF), tobacco smoking, plasma LDL-cholesterol concentration, and consumption of drugs were evaluated by multiple linear regression analysis. Aging was the major risk factor, followed by exposure to occupational noise and the presence of VWF. Plasma LDL-cholesterol concentration and the use of antihypertensive drugs also correlated significantly with SNHL. These main factors were able to explain about 28% of the SNHL variance. Additional factors in the analysis, including smoking, systolic and diastolic blood pressure, and consumption of salicylates did not significantly contribute to the genesis of SNHL.

Topics: Age Factors; Agricultural Workers' Diseases; Antihypertensive Agents; Auditory Threshold; Blood Pressure; Cholesterol, LDL; Hearing Loss, Noise-Induced; Humans; Male; Risk Factors; Salicylates; Smoking; Time Factors; Vibration

The interaction of noise with a variety of other agents and with some physical characteristics of the individual to produce noise-induced hearing loss is reviewed critically. The review is restricted, for the most part, to publications since 1970. Other agents interacting with steady-state noise that are reviewed here include: (1) ototoxic drugs (kanamycin, neomycin, ethacrynic acid, furosemide, and salicylates), (2) impulse noise, and (3) whole-body vibration. Physical characteristics of the individual that are reviewed are: (1) age, (2) presence of previous hearing loss from prior noise exposure, (3) eye color, and (4) race. Suggestions for future research in this general area are also made. Some of these suggestions are as follows: (1) to extend studies of the interaction of steady-state noise with impulse noise, salicylates, and whole-body vibration to encompass a broader range of exposure conditions, including exposure conditions typically encountered by the worker, (2) to develop an animal model of presbycusis to explore the interactions of noise-induced hearing loss and presbycusis, and (3) to explore the potential interactions resulting from concurrent exposure to multiple agents, such as impulse noise and ototoxic drugs, in younger, more susceptible animals.

Topics: Acoustic Stimulation; Age Factors; Animals; Ethacrynic Acid; Eye Color; Furosemide; Hearing Loss, Noise-Induced; Hearing Loss, Sensorineural; Humans; Kanamycin; Melanins; Neomycin; Presbycusis; Risk; Salicylates; Vibration

Diverse therapeutic agents, such as certain antibiotics, diuretics, and analgesics can cause functional and morphological damage to the inner ear. Noise present in recreational or occupational environment may also be potentially damaging to the auditory system when combined with some ototoxic therapeutic agents. This article documents recent research and controversies about the site and mechanism of action of major ototoxic drugs, noise-drug interaction, and possible prophylaxis against such ototoxicity.

Topics: Adult; Aminoglycosides; Animals; Anti-Bacterial Agents; Child; Cochlea; Diuretics; Drug-Related Side Effects and Adverse Reactions; Environmental Pollutants; Female; Guinea Pigs; Hair Cells, Auditory; Hair Cells, Auditory, Inner; Hearing Disorders; Hearing Loss, Noise-Induced; Humans; Infant, Newborn; Kanamycin; Organ of Corti; Quinine; Risk; Salicylates

Topics: Adult; Age Factors; Aged; Arthritis, Rheumatoid; Audiometry; Ear; Ear Diseases; Ear, Middle; Hearing Disorders; Hearing Loss, Noise-Induced; Hearing Tests; Humans; Indomethacin; Meniere Disease; Middle Aged; Neuritis; Pilot Projects; Salicylates