Hearing Loss In Rats Research Articles

The Effect of Thymoquinone on Acoustic Trauma-Induced Hearing Loss in Rats.

Background The aim of this study was to investigate the protective effect of thymoquinone, an antioxidant, on hearing loss induced by acoustic trauma in rats. Material and methods This study included 32 Wistar Albino rats divided into four groups: control, acoustic trauma, thymoquinone + acoustic trauma, and thymoquinone only, with eight rats per group. The control group received 0.5 mL of corn oil intraperitoneally for 10 days. The acoustic trauma group was exposed to 100 dB white noise at 4 kHz for 16 hours. The thymoquinone + acoustic trauma group received thymoquinone (10 mg/kg) intraperitoneally for two days before acoustic trauma and eight days after acoustic trauma. The thymoquinone only group received thymoquinone (10 mg/kg) for 10 days. Distortion product otoacoustic emissions (DPOAEs) were measured before and after treatments on days 1, 4, and 10. Results In the control group, DPOAE measurements showed no significant change over the study period. The acoustic trauma group exhibited a significant decrease in DPOAE on the first day after trauma, followed by some recovery. The thymoquinone + acoustic trauma group showed no significant decrease in DPOAE on the first day post-trauma, suggesting a protective effect. The thymoquinone only group also indicated no significant change in DPOAE measurements, suggesting that thymoquinone alone did not affect hearing function. Conclusion Thymoquinone demonstrated a protective effect against acoustic trauma-induced hearing loss in rats, as evidenced by stable DPOAE measurements post-trauma. These findings suggest that thymoquinone may help preserve hearing function by reducing oxidative stress in the cochlea. Further studies are needed to confirm these results in humans and optimize dosage and treatment protocols.

Early transtympanic administration of rhBDNF exerts a multifaceted neuroprotective effect against cisplatin-induced hearing loss.

Cisplatin-induced sensorineural hearing loss is a significant clinical challenge. Although the potential effects of brain-derived neurotrophic factor (BDNF) have previously been investigated in some ototoxicity models, its efficacy in cisplatin-induced hearing loss remains uncertain. This study aimed to investigate the therapeutic potential of recombinant human BDNF (rhBDNF) in protecting cells against cisplatin-induced ototoxicity. Using an in vivo model of cisplatin-induced hearing loss, we investigated the beneficial effects of transtympanic administration of rhBDNF in a thermogel solution on hearing function and cochlear injury, using electrophysiological, morphological, immunofluorescence and molecular analyses. Our data showed that local rhBDNF treatment counteracted hearing loss in rats receiving cisplatin by preserving synaptic connections in the cochlear epithelium and protecting hair cells (HCs) and spiral ganglion neurons (SGNs) against cisplatin-induced cell death. Specifically, rhBDNF maintains the balance of its receptor levels (pTrkB and p75), boosting TrkB-CREB pro-survival signalling and reducing caspase 3-dependent apoptosis in the cochlea. Additionally, it activates antioxidant mechanisms while inhibiting inflammation and promoting vascular repair. Collectively, we demonstrated that early transtympanic treatment with rhBDNF plays a multifaceted protective role against cisplatin-induced ototoxicity, thus holding promise as a novel potential approach to preserve hearing in adult and paediatric patients undergoing cisplatin-based chemotherapy.

Investigating the effects of hearing loss in rats and guinea pigs

Experimentally induced hearing loss in laboratory animals can lead to subsequent changes in the central nervous system. These central changes following hearing loss may lead to alterations in cognition and anxiety. In our laboratory, rats and guinea pigs are used to study the effects of cochlear trauma with the selected species dependent on the parameters of interest. Guinea pigs’ relatively large and easily accessible cochlea makes the species well suited for cochlear physiological and neural measurements, whereas rats have the advantage of well-established performance on a wide variety of behavioral tests. In a recent study, we investigated whether these well-established tests in rats for stress (open field test; OFT), and learning and memory (novel object recognition; NOR; Morris Water Maze; MWM) could be used in guinea pigs to investigate changes in behavior following conductive hearing loss. Analysis showed that guinea pigs could be trained in the MWM, and showed a similar range of behaviors as described for rats in OFT; however, NOR tests could not be interpreted as most guinea pigs did not interact with the novel objects. Overall, anxiety, spatial learning, and memory were not affected by 8 weeks of conductive hearing loss.

Protective and Therapeutic Effect of Platelet-Rich Plasma on Experimental Cisplatin Ototoxicity.

Cisplatin is a chemotherapeutic agent with an ototoxic effect that is frequently used in head and neck cancers. There are studies in the literature conducted with various antioxidant substances to protect and/or prevent ototoxicity. This study aims to investigate whether platelet-rich plasma (PRP) has a protective and therapeutic effect on cisplatin ototoxicity. A total of 40 Sprague Dawley albino rats were divided into six groups as control group (n=6), PRP-only group (n=6), cisplatin group (n=6), cisplatin + PRP group (n=6), PRP + cisplatin group (n=6), and donor group (n=10). At the beginning of the study and the 8th day, they were tested with distortion product otoacoustic emission (DPOAE). Assessment of DPOAE results was based on the signal-to-noise ratio in 2000, 3000, 4000, 6000, and 8000 Hz frequency bands. On the 8th day, the rats were sacrificed. For histological examinations, the temporal bones were dissected and fixed. After hematoxylin and eosin staining, the tissues were evaluated by light microscopy. In the DPOAE tests performed on the 0th and 8th days of the cisplatin group, it was observed that cisplatin caused hearing loss in the rat ears. It was determined that the cisplatin group at 2000 Hz, 3000 Hz and 4000 Hz had a significant decrease in hearing compared to all groups (p<0.015), while the cisplatin group at 6000 and 8000 Hz was characterized by hearing loss at a higher rate than all groups (p<0.001). At the end of the study, negative effects of cisplatin on both cellular dimensions (cytoplasmic vacuolization, cell degeneration, dilatation, apoptotic cells, nerve degeneration) and hearing function were observed. No protective or therapeutic effect of PRP on cisplatin ototoxicity was observed. Our study showed that platelet-rich plasma did not have a significant effect in the treatment of hearing loss due to cisplatin ototoxicity and in preventing hearing loss in rats.

Single Fraction and Hypofractionated Radiation Cause Cochlear Damage, Hearing Loss, and Reduced Viability of Merlin-Deficient Schwann Cells.

Vestibular schwannomas (VS) are benign intracranial tumors caused by loss of function of the merlin tumor suppressor. We tested three hypotheses related to radiation, hearing loss (HL), and VS cell survival: (1) radiation causes HL by injuring auditory hair cells (AHC), (2) fractionation reduces radiation-induced HL, and (3) single fraction and equivalent appropriately dosed multi-fractions are equally effective at controlling VS growth. We investigated the effects of single fraction and hypofractionated radiation on hearing thresholds in rats, cell death pathways in rat cochleae, and viability of human merlin-deficient Schwann cells (MD-SC). Adult rats received cochlear irradiation with single fraction (0 to 18 Gray [Gy]) or hypofractionated radiation. Auditory brainstem response (ABR) testing was performed for 24 weeks. AHC viabilities were determined using immunohistochemistry. Neonatal rat cochleae were harvested after irradiation, and gene- and cell-based assays were conducted. MD-SCs were irradiated, and viability assays and immunofluorescence for DNA damage and cell cycle markers were performed. Radiation caused dose-dependent and progressive HL in rats and AHC losses by promoting expression of apoptosis-associated genes and proteins. When compared to 12 Gy single fraction, hypofractionation caused smaller ABR threshold and pure tone average shifts and was more effective at reducing MD-SC viability. Investigations into the mechanisms of radiation ototoxicity and VS radiobiology will help determine optimal radiation regimens and identify potential therapies to mitigate radiation-induced HL and improve VS tumor control.

The potential therapeutic and/or protective effects of steroid, PRP and melatonin on noise-induced hearing loss in rats

The potential therapeutic and/or protective effects of steroid, PRP and melatonin on noise-induced hearing loss in rats

Ototoxicity of Triclosan: A Rat Model Study.

Triclosan is utilized as an antibacterial factor in many industrial products. Although there are many toxic features of triclosan in the literature, there is no study on the effect of triclosan on hearing. The purpose of this study is to determine the effect of triclosan on hearing in rats. In this prospective, experimental animal study, 40 healthy Sprague-Dawley rats with normal response to the distortion-product otoacoustic emission (DPOAE) measurements were divided into four groups. Group 1, as the control group, was given only corn oil, group 2 was given 5 mg/kg triclosan dissolved in corn oil, group 3 was given 10 mg/kg triclosan dissolved in corn oil, and group 4 was given 100 mg/kg triclosan dissolved in corn oil; triclosan and corn oil were administered by oral gavage to all groups. In our study, low-dose triclosan did not cause hearing loss, but hearing loss was observed in the group that was given high-dose triclosan (100 mg/kg). These findings suggest that triclosan causes hearing loss in rats. This issue should be investigated further to avoid triclosan ototoxicity in humans.

Superoxide dismutase@zeolite Imidazolate Framework-8 Attenuates Noise-Induced Hearing Loss in Rats.

Reactive oxygen species (ROS) and inflammation have been considered major contributors to noise-induced hearing loss (NIHL) that constituted a public health threat worldwide. Nanoantioxidants, with high antioxidant activity and good stability, have been extensively used in the study of ROS-related diseases. In this study, we constructed a superoxide dismutase (SOD)@zeolite imidazolate framework-8 (ZIF-8) nanoparticle based on biomimetic mineralization and applied it to a rat model of NIHL. Our results showed that SOD@ZIF-8 effectively protected the animals from hearing loss and hair cell loss caused by noise. ROS, oxidative damage, and inflammation of noise-damaged cochlea were attenuated considerably after SOD@ZIF-8 administration. Importantly, we found that SOD@ZIF-8 achieved nanotherapy for NIHL in rats via a primary effect on the Sirtuin-3 (SIRT3)/superoxide dismutase2 (SOD2) signaling pathway without obvious adverse side effects. Therefore, our study is expected to open up a new field for NIHL treatment, and lay a foundation for the application of nanomaterials in other ROS-related inner ear diseases.

Pravastatin Administration Alleviates Kanamycin-Induced Cochlear Injury and Hearing Loss.

The effect of statins on aminoglycoside-induced ototoxicity is controversial. This study aimed to explore the role of pravastatin (PV) in kanamycin-induced hearing loss in rats. Adult rats were intraperitoneally treated with 20 mg/kg/day of kanamycin (KM) for 10 days. In the PV- and PV + KM-treated rats, 25 mg/kg/day of PV was intraperitoneally administered for 5 days. The auditory brainstem response (ABR) thresholds were measured before and after drug treatment using a smartEP system at 4, 8, 16, and 32 kHz. Cochlear changes in poly ADP-ribose (PAR) polymerase (PARP), PAR, and caspase 3 were estimated using Western blotting. PV administration did not increase the ABR thresholds. The KM-treated rats showed elevated ABR thresholds at 4, 8, 16, and 32 kHz. The PV + KM-treated rats demonstrated lower ABR thresholds than the KM-treated rats at 4, 8, and 16 kHz. The cochlear outer hair cells and spiral ganglion cells were relatively preserved in the PV + KM-treated rats when compared with that in the KM-treated rats. The cochlear expression levels of PARP, PAR, and caspase 3 were higher in the KM-treated rats. The PV + KM-treated rats showed lower levels of PARP, PAR, and caspase 3 than the KM-treated rats. PV protected cochleae from KM-induced hearing loss in rats. The regulation of autophagy and apoptosis mediated the otoprotective effects of PV.

Effect of Electroacupuncture on Noise-Induced Hearing Loss in Rats.

Acupuncture has long been used to relieve some inner ear diseases such as deafness and tinnitus. The present study examined the effect of electroacupuncture (EA) on noise-induced hearing loss (NIHL) in animals. A NIHL rat model was established. Electroacupuncture pretreatment at 2 Hz or posttreatment at the right Zhongzhu (TE3) acupoint was applied for 1 hour. Auditory thresholds were measured using auditory brainstem responses (ABRs), and histopathology of the cochlea was examined. The results indicated that the baseline auditory threshold of ABR was not significantly different between the control (no noise), EA-only (only EA without noise), noise (noise exposure only), pre-EA (pretreating EA then noise), and post-EA (noise exposure then posttreating with EA) groups. Significant auditory threshold shifts were found in the noise, pre-EA, and post-EA groups in the immediate period after noise exposure, whereas auditory recovery was better in the pre-EA and post-EA groups than that in the noise group at the three days, one week (W1), two weeks (W2), three weeks (W3), and four weeks(W4) after noise stimulation. Histopathological examination revealed greater loss of the density of spiral ganglion neurons in the noise group than in the control group at W1 and W2. Although significant loss of spiral ganglion loss happened in pre-EA and post-EA groups, such loss was less than the loss of the noise group, especially W1. These results indicate that either pretreatment or posttreatment with EA may facilitate auditory recovery after NIHL. The detailed mechanism through which EA alleviates NIHL requires further study.

Effects of Androgen Receptor Inhibition on Kanamycin-Induced Hearing Loss in Rats.

Megalin has been proposed as an endocytic receptor for aminoglycosides as well as estrogen and androgen. We aimed to investigate the otoprotective effects of antiandrogens (flutamide, FM) on kanamycin (KM)-induced hearing loss in rats. Rats were divided into four groups. The KM group was administered KM (20 mg/kg/day) for 5 days, while the FM group received FM (15 mg/kg/day) for 10 days. In the KM + FM group, KM and FM (15 mg/kg/day) were simultaneously injected for 5 days and then FM was injected for 5 days. Auditory brainstem responses were measured. Western blotting and/or quantitative reverse transcriptase-polymerase chain reaction were performed for megalin, cytochrome P450 1A1 (Cyp1a1), Cyp1b1, metallothionein 1A (MT1A), MT2A, tumor necrosis factor (TNF)-α, caspase 3, and cleaved caspase 3. The FM + KM group showed attenuated auditory thresholds when compared with the KM group at 4, 8, 16, and 32 kHz (all p < 0.05). The KM + FM group showed lower megalin and Cyp1b1 levels than the KM group (all p < 0.05). The KM + FM group revealed lower MT1A, TNFα, and caspase 3 protein levels, compared with those in the KM group (all p < 0.05). Androgen receptor inhibition protects against cochlear injuries in KM-induced hearing loss rats by attenuating megalin expression, revealing anti-inflammatory and anti-apoptotic effects.

Combination photobiomodulation/N-acetyl-L-cysteine treatment appears to mitigate hair cell loss associated with noise-induced hearing loss in rats.

Sensorineural hearing loss is an intractable disease. Acoustic overstimulation creates hearing loss; many patients exhibit social and emotional dysfunctions. In a model of noise-induced hearing loss (NIHL), low-level laser photobiomodulation (PBM) at a near-infrared wavelength significantly improved auditory brainstem response (ABR) thresholds. In addition, both N-acetyl-L-cysteine (NAC) and acetyl-L-carnitine (ALCAR) attenuated NIHL, reducing the effects of noise trauma in the cochlea and the central auditory system. Here, we combined PBM with antioxidants to explore hearing threshold recovery and morphological hair cell changes after rats were exposed to noise. The average auditory brainstem response thresholds after PBM/NAC combination treatment were reduced from the apex to the basal turn at all of 8, 16, and 32 kHz compared to the noise-only group. The PBM/NAC combination treated group exhibited intact outer hair cells in all turns, and significantly greater hair cell numbers in the middle and basal cochlear turns, than did controls. Thus, PBM/NAC treatment may prevent hearing dysfunction caused by NIHL.

Effects of Co-Exposure to Noise and JP-4 Jet Fuel on Hearing Loss in Rats

Effects of Co-Exposure to Noise and JP-4 Jet Fuel on Hearing Loss in Rats

Tauroursodeoxycholic acid attenuates cisplatin-induced hearing loss in rats

Tauroursodeoxycholic acid (TUDCA) has been reported to be protective against apoptosis and oxidative stress in various cell types. A few studies have demonstrated otoprotective effects of TUDCA in mouse models. This study investigated the otoprotective effects of TUDCA in cisplatin (CXP)-induced hearing-loss rats. Eight-week-old female Sprague-Dawley rats were used. The CXP group received intraperitoneal injection of CXP at a dose of 5 mg/kg from day 1 to day 3. The CXP + TUDCA group received an intraperitoneal injection of 5 mg/kg CXP and 100 mg/kg TUDCA from day 1 to day 3. The mRNA expression levels of heme oxygenase 1 (HO1) and superoxide dismutase 2 (SOD2) were measured, and the protein levels of caspase 3, cleaved caspase 3, and aryl hydrocarbon receptor (AhR) were evaluated. The CXP group demonstrated higher mean auditory brainstem responses (ABR) thresholds than the control group. The mean ABR threshold shifts were lower in the CXP + TUDCA group than in the CXP group. The CXP group showed elevated HO1 and SOD2 mRNA expression levels compared to the control group, but these changes were reversed in the CXP + TUDCA group. Compared to the levels in the control group, caspase 3, cleaved caspase 3, and AhR levels were higher in the CXP group, but the increase in cleaved caspase-3 was attenuated in the CXP + TUDCA group. The cochlea showed a higher number of spiral ganglion cells and outer hair cells in the CXP + TUDCA group than in the CXP group. TUDCA reduced CXP-induced hearing loss in adult rats. The HO1-mediated antioxidative effects attenuated apoptosis in the cochlea, but AhR activation was not reversed.

Bilateral Carotid Artery Occlusion and Cochlear Oxidative Stress and Hearing Loss in Rats.

Introduction:This study aimed to evaluate the effects of bilateral carotid artery occlusion on cochlear oxidative stress and hearing status in rats.Methods:The rats were divided into two sets. The first set was used for electrophysiological recording (click and 4 kHz tone burst auditory brainstem responses and electrocochleography) on the day before surgery and then on the first, fourth, and seventh days after surgery. Animals of the second set were used for biochemical analysis. The cochlea of animals in the second set was collected on the first, fourth, and seventh days after carotids occlusion for biochemical analysis. For the control groups, no carotids occlusion was done. For ischemia induction, both common carotid arteries were occluded for 20 minutes.Results:Electrophysiological analysis showed that burst auditory brainstem thresholds significantly elevated after common carotid arteries occlusion on the first, fourth, and seventh days after surgery with abnormal electrocochleography results at 75%, 70%, and 85% on the first, fourth, and seventh days after surgery, respectively. The electrophysiological finding confirmed by biochemical results that showed malondialdehyde and nitric oxide levels increased and superoxide dismutase and catalase activities decreased after occlusion in cochlea tissue.Conclusion:This study showed that bilateral common carotid artery occlusion increases cochlear oxidative stress and induces hearing loss in rats.

The Sub-acute Effect of Lead Exposure on the Auditory Brainstem Response in Male Rats

Background: Lead is a major environmental pollutant and can adversely affect humans and animals. There are conflicting data about the ototoxic effect of lead. This study experimentally examined the association between blood lead levels (BLL) and the subsequent hearing impairment in male rats. Methods: Twenty-two male rats were randomly categorized into experimental (exposed to lead acetate, 4 mg/kg by gavage) and control groups. We evaluated the groups by click and tone audiometric burst tests, comparing the data before and 30 days after exposure to lead acetate (4mg/kg). Also, blood samples were collected from the rats and analyzed for lead levels by graphite furnace atomic absorption spectrometry. Results: The study findings demonstrated remarkable increase in hearing threshold in the lead-exposed group, compared to the controls (p&lt;0.0001). Also, the blood lead levels revealed a significant association of lead acetate with the hearing loss in rats. Conclusion: This study revealed that exposure to lead acetate can be damaging to hearing. However, future research is recommended to clarify the mechanism of action of lead toxicity on the auditory function at varying blood lead concentrations.

Microglial activation in the cochlear nucleus after early hearing loss in rats

ObjectiveMicroglia are highly specialized tissue macrophages in the central nervous system. Their activation in the auditory system has been reported in adult hearing loss models, but their status in the developing auditory system is less understood. Therefore, we investigated microglial status in the cochlear nucleus (CN) during normal developing periods and after exposing rats to amikacin, a potent ototoxin, around the time of hearing onset. MethodsTo develop the deafness model, rats were administered with a daily intraperitoneal injection of amikacin (500 mg/kg) from postnatal day 7 (P7) to P15. To evaluate the expression of ionized calcium binding adaptor molecule 1 (Iba1), we performed immunohistochemical analysis using rat brains from P10–60. To compare the expression of microglia-related gene, reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis were performed. ResultsImmunohistochemical analysis revealed that, under normal conditions, microglia had relatively large cell bodies with several extended processes that surrounded other cells at P10, while the sizes and number of these cells gradually decreased afterward. In contrast, when amikacin was administered from P7 to P15, microglia maintained large cell bodies with relatively shorter processes at both P15 and P21. Furthermore, RT-qPCR analysis revealed upregulation of genes including phagocytotic and anti-inflammatory markers after amikacin administration. ConclusionThese results suggest that microglia are activated in the CN, and they may contribute to tissue remodeling after early hearing loss in the developing auditory system.

SENS-401 Effectively Reduces Severe Acoustic Trauma-Induced Hearing Loss in Male Rats With Twice Daily Administration Delayed up to 96 hours.

SENS-401 (R-azasetron besylate) is effective against severe acoustic trauma-induced hearing loss. SENS-401 has calcineurin inhibiting properties and attenuates cisplatin-induced hearing loss in a rat model. Cisplatin-induced and acoustic trauma-induced hearing loss share common apoptotic pathways. The dose-response relationship of SENS-401 (6.6 mg/kg BID, 13.2 mg/kg BID, 26.4 mg/kg QD) and treatment time-window (13.2 mg/kg BID starting 24, 72, and 96 h posttrauma) versus placebo for 28 days were evaluated in a male rat model of severe acoustic trauma-induced hearing loss (120 dB SPL, 2 h) using auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE) measures followed by cochlear outer hair cell (OHC) counting with myosin-VIIa immunolabeling. All SENS-401 doses improved ABR threshold shift and recovery, reaching statistical significance (p < 0.05) for ABR threshold recoveries after 28-days treatment. DPOAE amplitude loss and recovery improved markedly for 13.2 mg/kg BID SENS-401, reaching significance after 14 days (p < 0.05). Significant improvements in ABR threshold shifts/recovery and DPOAE amplitude loss occurred with up to 96-hours delay in initiating SENS-401 (p < 0.05), and in DPOAE amplitude recovery with up to 72-hours delay (p < 0.05). Significantly more surviving OHCs were present after SENS-401 treatment compared with placebo after 24 to 96-hours delay posttrauma, with up to 5.3-fold more cells in the basal cochlea turn. In vivo data support the otoprotective potential of twice daily oral SENS-401. Improvements in hearing loss recovery make SENS-401 a promising clinical candidate for acoustic trauma-induced hearing loss, including when treatment is not initiated immediately.

The protective effect of metformin against the noise-induced hearing loss.

To test the protective effect of metformin against noise-induced hearing loss. 24 rats were included in the study. The first group was exposed to noise only, the second group took metformin, the third group was exposed to noise and took metformin, and the fourth group was neither exposed to noise nor took metformin as control group. After measurement of baseline DPOAE and ABR of rats, the metformin group and the metformin + noise group received 300mg/kg/day metformin via gavage for 10days. On the 11th day, group 1 and group 3 were exposured to white noise at 105dB SPL for 15h. After noise exposure, DPOAE and ABR measurements of all rats were repeated on days 1st, 7th, and 21st. At the end of the study, all animals were sacrificed and cochlear tissues were separated for immunohistochemical assessments. ABR threshold values and DPAOE measurements of groups 1 and 3 were deteriorated on the 1st day after noise, while deterioration in group 1 continued on 7th and 21st days, but normalized on 7th day in group 3. After immune staining, a significant immunoreaction was observed in the noise group, while the reaction in the noise + metformin group was close to the control group. Metformin has a protective effect on noise-induced hearing loss in rats. As a conclusion, it is determined that metformin protects from permanent threshold shift in rats. It can be considered a good alternative for protecting noise-induced hearing loss.

The Effects of Normobaric Hyperoxia Pre- and Post-treatment on the Development of Noise-Induced Hearing Loss in Rats

Background: Occupational noise exposure is one of the leading factors for developing noise-induced hearing loss (NIHL), particularly among workers worldwide. The literature review reveals that beside conventional strategies for preventing NIHL, multiple interventions can be applied to reduce or prevent such disorders. The present study aimed to investigate the preventive effects of normobaric hyperoxia pre- and post-treatment on the development of NIHL in rats. Methods: Four groups of male Wistar rats were exposed to pure oxygen alone, noise alone, or oxygen plus noise for 6 hours a day, 5 days a week for 4 weeks. One group served as the control and received neither noise nor oxygen. Animals in the noise groups were exposed to high-pass white noise of 100 dB SPL, centred at 8 KHz. The treatment protocols were based on inhalation of pure normobaric oxygen (95%) for 3 hours in a chamber either before or after noise exposure. The auditory brainstem responses (ABRs) for click and 4, 6, 8, 12, and 16 kHz stimuli, as well as distortion product otoacoustic emissions (DPOAEs) at 4, 6, 8, and 10 kHz, were recorded to assess the level of hearing impairment before exposure and 4 weeks post-exposure. Results: The results showed that pre-treatment of rats with 3 hours of normobaric hyperoxia contributed to a significant reduction in ABR threshold shifts, while improving the DPOAE amplitudes (P 0.05). Conclusions: Pre- and post-treatment with normobaric hyperoxia seem to produce protective effects through either boosting cellular oxygenation or maximizing antioxidant enzyme activities and tolerance against noise-induced ischemia and hypoxia in the cochlea. Therefore, application of normobaric hyperoxia pre- or post-treatment, along with other conventional protective strategies, can be helpful in the fight against NIHL.