Influence of noise exposure on antioxidant system and TEOAEs in rabbits (original) (raw)
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Introduction: Cochlear noise injury is considered one of the most debilitating diseases worldwide. Numerous drug trials have been made for complete protection from this acoustic trauma, unfortunately with little success. Recently, drug combination has showed promising effects in treating this trauma; however, this has to be further documented by in-depth researches. Aim of the work: To estimate the effect of combination of the antioxidants; vitamins A, C and E, plus magnesium (A, C, E+ Mg) in either protection or treatment of noise-induced cochlear injury in adult guinea pigs. Materials and methods: Twenty five guinea pigs were used in this study and were divided equally into five groups. Group I served as a control group. Group II administered the drug combination for 5 successive days. Group III exposed once to 120 dBSPL octave band noise for 5 successive hours. Group IV pre-treated with vitamins A, C, E+ Mg for 5 successive days prior to noise exposure. Group V first exposed to same noise injury, and then same drug combination was administered for 5 successive days, starting one day after noise exposure. Results: Noise exposure resulted in profound cochlear damage. Prophylactic administration of the drug combination showed partial protection of the cochlea as detected audiologically and histologically. In contrast, significant improvement of both function and structure of the cochlea was revealed with post-treatment 1 day after noise-induced cochlear damage. Conclusion: Delayed treatment by this combination of drugs (vitamins A, C, E+ Mg) proved to be effective even if started one day after noise exposure. However, drug combination used as prophylactic treatment was not as effective. [Nagwa Kostandy Kalleny, Nevine Bahaa E. Soliman and Rasha Elkabarity Synergistic Effect of combined antioxidants on Noise-Induced Acoustic Trauma in Adult Guinea Pigs. Audiological and Histological Study]
Glutathione limits noise-induced hearing loss
Hearing Research, 2000
The generation of reactive oxygen species (ROS) is thought to be part of the mechanism underlying noise-induced hearing loss (NIHL). Glutathione (GSH) is an important cellular antioxidant that limits cell damage by ROS. In this study, we investigated the effectiveness of a GSH supplement to protect GSH-deficient animals from NIHL. Pigmented guinea pigs were exposed to a 4 kHz octave band noise, 115 dB SPL, for 5 h. Group 1 had a normal diet, while groups 2, 3 and 4 were fed a 7% low protein diet (leading to lowered tissue levels of GSH) for 10 days prior to noise exposure. One hour before, immediately after and 5 h after noise exposure, subjects received either an intraperitoneal injection of 5 ml/kg body weight of 0.9% NaCl (groups 1 and 2), 0.4 M glutathione monoethyl ester (GSHE; group 3) or 0.8 M GSHE (group 4). Auditory thresholds were measured by evoked brain stem response at 2, 4, 8, 12, 16 and 20 kHz before and after noise exposure. Ten days post exposure, group 1 showed noise-induced threshold shifts of approximately 20 dB at 2, 16 and 20 kHz and 35 to 40 dB at other frequencies. Threshold shifts in group 2 were significantly greater than baseline at 2, 4, 16 and 20 kHz. GSHE supplementation in a dose-dependent fashion attenuated the threshold shifts in the low protein diet animals. Hair cell loss, as evaluated with cytocochleograms, was consistent with the auditory-evoked brainstem response results. Group 2 exhibited significantly more hair cell loss than any of the other groups; hair cell loss in group 3 was similar to that seen in group 1; group 4 showed less loss than group 1. These results indicate that GSH is a significant factor in limiting noiseinduced cochlear damage. This is compatible with the notion that ROS generation plays a role in NIHL and that antioxidant treatment may be an effective prophylactic intervention.
The Laryngoscope, 2004
The objective was to investigate the effects of both noise exposure and ascorbic acid on oxidative status and hearing thresholds of rabbits. Study Design: Randomized prospective animal study comparing oxidative parameters and otoacoustic emissions in two rabbit groups exposed to noise. One group was given absorbic acid, the other group was not given any treatment. Methods: Two groups of rabbits were used in the study; each group had six rabbits. The six rabbits in the first group were not given any treatment, whereas 500 mg intramuscular ascorbic acid twice daily for 2 1 ⁄2 days was given to the six rabbits in the second group. Transient evoked otoacoustic emissions were recorded in all animals before and after noise exposure. Total protein sulfhydryl groups, carbonyl contents, and malondialdehyde levels, as well as erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels, were measured in all rabbits. All the rabbits were exposed to noise (100 dB sound pressure level, 1000 Hz, 1 h), and transient evoked otoacoustic emissions were recorded again. Results: When oxidative parameters before noise exposure were compared, erythrocyte glutathione and catalase enzyme levels were detected to be higher in the second group (P < .05). In the first group of rabbits after noise exposure, total protein sulfhydryl groups were found to be reduced (P < .05), whereas plasma carbonyl contents and malondialdehyde levels were elevated significantly (P < .05). In this group, erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels were low (P < .05). In the second group, which was given ascorbic acid, total protein sulfhydryl groups were reduced (P < .05), whereas plasma carbonyl contents and malondialdehyde levels did not change (P > .05) following noise exposure. In the second group, erythrocyte glu-tathione and catalase enzyme levels were reduced (P < .05), but superoxide dismutase levels did not change (P > .05). Transient evoked otoacoustic emissions after noise exposure were weak in both groups, but reproducibility and signal-to-noise ratios were higher in the second group (P < .05). Conclusion: Ascorbic acid treatment inhibited both lipid peroxidation and oxidative damage of proteins in rabbits exposed to noise. The study data suggest, at least, that oxidative status should be included in the physiopathology of noise-induced hearing loss; in addition, a brief application of ascorbic acid before noise exposure appeared to play a protective role for cochlea.
Role of glutathione in protection against noise-induced hearing loss
Brain Research, 1998
. A potential mechanism of hearing loss due to acoustic overstimulation is the generation of reactive oxygen species ROS . ROS not removed by antioxidant defenses could be expected to cause significant damage to the sensory cells of the cochlea. We studied the Ž . w x Ž . influence of the antioxidant glutathione GSH on noise-induced hearing loss by using L-buthionine-S, R -sulfoximine BSO , an inhibitor Ž . of GSH synthesis, and 2-oxothiazolidine-4-carboxylate OTC , a cysteine prodrug, which promotes rapid restoration of GSH when GSH Ž . is acutely depleted. Pigmented female guinea pigs were exposed to broadband noise 102 dB SPL, 3 hrday, 5 days while receiving daily injections of BSO, OTC, or saline. By weeks 2 and 3 after noise exposure, BSO-treated animals showed significantly greater threshold shifts above 12 kHz than saline-treated subjects, whereas OTC-treated animals showed significantly smaller threshold shifts at 12 kHz than controls. Histologically assessed noise-induced damage to the organ of Corti, predominantly basal turn row 1 outer hair cells, was most pronounced in BSO-treated animals. High performance liquid chromatographic analysis showed that OTC significantly increased cysteine levels, but not GSH levels, in the cochlea. These findings show that GSH inhibition increases the susceptibility of the cochlea to noise-induced damage and that replenishing GSH, presumably by enhancing availability of cysteine, attenuates noise-induced cochlear damage. q 1998 Elsevier Science B.V.
Open Access Library Journal, 2021
This is a detailed experimental and comparative study evaluating the harmful effects of graded loud noise on hematological and antioxidant in Wistar albino rats. Wistar albino rats were divided into a control group (those kept away from the noise due to a generator set), groups 1 (exposed to varied, 85 - 105 db levels of loud noise from a generator) and groups 2 (exposed to less, 40 - 55 db levels of loud noise from generator set) and exposed to way off fumes from electrical generator sounds at different sound level for 8 hours each day for 28 days. The result indicated that activities and concentrations of the antioxidant enzymes: glutathione peroxidase, catalase and glutathione increased significantly (p < 0.05) when compared with the control group in group 1. There was also an increase in the concentrations of malondialdehyde and hematological parameters (RBC, WBC, PCV, hemoglobin, platelets) among the rats exposed to loud noise from a generator set in group 2, when compared t...
Journal of Neuroscience, 2013
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 Q 10 analog (Q ter ) was used. We analyzed auditory function, cochlear oxidative stress, morphological alterations in auditory cortices and cochlear structures, and levels of coenzymes Q 9 and Q 10 (CoQ 9 and CoQ 10 , 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 CoQ 10 analog reduced oxidative-induced cochlear damage, hearing loss, and cortical dendritic injury. Furthermore, cochlear levels of CoQ 9 and CoQ 10 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.
Protective effects of N-acetylcysteine on noise-induced hearing loss in guinea pigs
Acta otorhinolaryngologica Italica : organo ufficiale della Società italiana di otorinolaringologia e chirurgia cervico-facciale, 2009
Increasing evidence suggests the involvement of oxidative stress in noise-induced hearing loss. The present study analysed, in an animal experimental model, the time course of the pathogenic mechanisms of noise-induced cochlear damage and the efficacy of the antioxidant drug N-acetylcysteine in reducing noise ototoxicity. Animals were divided into two groups, exposed to noise one treated with N-acetylcysteine for 3 days and one (the control group) with saline. Acoustic trauma was induced by a continuous pure tone of 6 kHz, at 120 dB SPL for 30 minutes. Electrocochleographic recordings were made from an implanted round window electrode and the compound action potentials were measured daily at 2-16 kHz for 7 days. Morphological changes were analysed by scanning electron microscopy. The acoustic threshold measured 1 hour after acoustic trauma was elevated in the control group to 70-90 dB in the higher frequencies of the compound action potential audiogram, with a maximum threshold elev...
Oxidative stress pathways in the potentiation of noise-induced hearing loss by acrylonitrile
Hearing Research, 2007
We hypothesize that the disruption of antioxidant defenses is a key mechanism whereby chemical contaminants can potentiate noise-induced hearing loss (NIHL). This hypothesis was tested using acrylonitrile (ACN), a widely used industrial chemical whose metabolism is associated with glutathione (GSH) depletion and cyanide (CN) generation. CN, in turn, can inhibit Cu/Zn superoxide dismutase (SOD). We have shown previously that ACN potentiates NIHL, even with noise exposure approaching permissible occupational levels. However, the relative involvement of GSH depletion and/or CN production in this potentiation is still unknown. In this study, we altered these metabolic pathways pharmacologically in order to further delineate the role of specific antioxidants in the protection of the cochlea. We investigated the effects of sodium thiosulfate (STS), a CN inhibitor, 4-methylpyrazole (4MP), a drug that blocks CN generation by competing with CYP2E1, and L-N-acetylcysteine (L-NAC), a pro-GSH drug, in order to distinguish between GSH depletion and CN production as the mechanism responsible for potentiation of NIHL by ACN. Long-Evans rats were exposed to an octave-band noise (97 dB SPL, 4 h/day, 5 days) and ACN (50 mg/kg). Separate pre-treatments with STS (150 mg/kg), 4MP (100 mg/kg) and L-NAC (4 · 400 mg/kg) all dramatically reduced blood CN levels, but only L-NAC significantly protected GSH levels in both the liver and the cochlea. Concurrently, only L-NAC treatment decreased the auditory loss and hair cell loss resulting from ACN + noise, suggesting that GSH is involved in the protection of the cochlea against reactive oxygen species generated by moderate noise levels. On the other hand, CN does not seem to be involved in this potentiation. Published by Elsevier B.V.
The Effects of Noise on Hearing and Oxidative Stress in Textile Workers
The aim of this study was to investigate the effects of noise on hearing, lipid peroxidation and antioxidant enzymes in textile workers. Thirty textile workers exposed to high noise 105 dB (A) in a textile factory, and 30 healthy male volunteers in our hospital as a control group were included in the study. In both groups, following audiometric tests, blood samples were obtained. In these blood samples, Malonydialdehyte (MDA), Superoxide dismutase (SOD) and Catalase (CAT) levels were investigated. Statistical analysis was performed by using SPSS version 11.0 (SPSS Inc., Chicago 1L) software program. Mean pure tone audiometric thresholds in workers were significantly higher than in control subjects at frequencies 2,000, 4,000 and 6,000 Hz (p<0.05). Hearing losses were more evident at high frequencies (4-6 kHz) than at low frequencies in worker group. (p<0.05). It was observed that textile workers with longer employment duration had poorer hearing threshoulds and the hearing loss had started on those who had worked for 5-8 yr. While MDA levels were significantly higher in workers than controls (p<0.001), CAT activity was significantly lower (p<0.005). Also, SOD activity was lower in workers but difference was not statistically significant. We observed a significant change in hearing threshold of the textile workers compared with that of the control group. Increase in MDA level and decreases in CAT and SOD activities in textile workers, support the opinion that the noise causes the oxidative stress. The fact that noise both causes hearing loss and increases oxidative stress suggests that there may be a relationship between the oxidative stress and hearing loss. But, further studies are needed in order to verify this opinion.