The therapeutic effect of thymoquinone on acoustic trauma-induced hearing loss in rats (original) (raw)
Related papers
Thymoquinone treatment for inner-ear acoustic trauma in rats
The Journal of laryngology and otology, 2015
To investigate whether thymoquinone has any eliminative effects against inner-ear damage caused by acoustic trauma. Thirty-two male rats were divided into four groups. Group 1 was only exposed to acoustic trauma. Group 2 was given thymoquinone 24 hours before acoustic trauma and continued to receive it for 10 days after the trauma. Group 3 was only treated with thymoquinone, for 10 days. Group 4, the control group, suffered no trauma and received saline instead of thymoquinone. Groups 1 and 2 were exposed to acoustic trauma using 105 dB SPL white noise for 4 hours. There was a significant decrease in distortion product otoacoustic emission values and an increase in auditory brainstem response thresholds in group 1 on days 1, 5 and 10, compared with baseline measurements. In group 2, a decrease in distortion product otoacoustic emission values and an increase in auditory brainstem response threshold were observed on day 1 after acoustic trauma, but measurements were comparable to bas...
An Evaluation of the Protective Effects of Thymoquinone on Amikacin-Induced Ototoxicity in Rats
Clinical and Experimental Otorhinolaryngology, 2015
Objectives. In this study we investigated the probable protective effects of thymoquinone on amikacin-induced ototoxicity in rats. Methods. Thirty-two healthy rats were divided into four groups (amikacin, amikacin+thymoquinone, thymoquinone, and no treatment). Thymoquinone was fed to the rats via oral gavage in a dose of 40 mg/kg/day throughout the study period of 14 days. Amikacin was given by the intramuscular route in a dose of 600 mg/kg/day. Audiological assessment was conducted by the distortion product otoacoustic emission (DPOAE) and auditory brainstem response (ABR) tests, administered to all rats at the beginning of the study, and also on days 7 and 15. Biochemical parameters were calculated at the termination of the study to evaluate the oxidative status. Results. There were significant decreases in DPOAE values and significant increases in ABR thresholds of the amikacin group on days 7 and 15, as compared to the amikacin+thymoquinone group. While ABR thresholds of the amikacin group increased significantly on days 7 and 15 as compared to their initial values, there were no significant differences between the initial and the 7th and 15th day values of ABR thresholds in the amikacin+thymoquinone group. Total oxidant status and oxidative stress index values of the amikacin+thymoquinone group were significantly lower than those of the amikacin group. Total antioxidant status values of the amikacin+thymoquinone group were significantly higher than those of the amikacin group. Conclusion. Our study has demonstrated that the ototoxic effect brought forth by amikacin could be overcome with the concurrent use of thymoquinone.
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]
Protective effect of thymoquinone against cisplatin-induced ototoxicity
European Archives of Oto-Rhino-Laryngology, 2013
The aim of this study was to investigate the potential protective effect of thymoquinone against cisplatin-induced ototoxicity. This study is a prospective, controlled experimental animal study. Experiments were performed on 30 healthy female Sprague-Dawley rats. Thirty animals were divided into three groups of 10 animals each. Group 1 received an intraperitoneal (i.p.) injection of cisplatin 15 mg/kg. Group 2 received i.p. thymoquinone 40 mg/kg/day for 2 days prior to cisplatin injection and third day i.p. cisplatin 15 mg/kg was administered concomitantly. Group 2 continued to receive i.p. thymoquinone until fifth day. Group 3 received i.p. thymoquinone 40 mg/kg/day for 5 days. Pretreatment distortion product otoacoustic emissions (DPOAE) and auditory brain stem responses (ABR) testing from both ears were obtained from the animals in all groups. After the baseline measurements, drugs were injected intraperitonally. After an observation period of 3 days, DPOAE measurements and ABR testing were obtained again and compared with the pretreatment values. There was no statistically significant difference between pre and posttreatment DPOAE responses and ABR thresholds group 2 and 3. However, group 1 demonstrated significant deterioration of the ABR thresholds and DPOAE responses. Our results suggest that DPOAE responses and ABR thresholds were preserved in the cisplatin plus TQ-treated group when compared with the group receiving cisplatin alone. According to these results, cisplatin-induced ototoxicity may be prevented by thymoquinone use in rats.
Antioxidant protection against acoustic trauma by coadministration of idebenone and vitamin E
Neuroreport, 2008
Idebenone, a synthetic analogue of coenzyme Q, attenuates noiseinduced hearing loss by virtue of its antioxidant properties. This study involves a guinea pig model of acoustic trauma where the e¡ectiveness of idebenone is analyzed in comparison with Vitamin E (a-tocopherol) that exhibits a potent antioxidant activity in the inner ear. Idebenone and vitamin E were injected intraperitoneally 1h 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 identi¢cation of missing and apoptotic cells was also performed. The results showed that the protective e¡ects of idebenone and vitamin E were not additive implying that the two antioxidants may share competitive mechanisms.
Medical Science Monitor, 2012
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. Material/Methods: 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.
2008
INTRODUCTION: In our study, relationship between hearing loss due to acoustic trauma and serum levels of vitamin B12, folic acid, zinc, magnesium and malondialdehyde were investigated. MATERIAL AND METHODS: The study was carried out on 135 healthy male individuals who were subjected to 138 dB sound intensity level. The mean age was 22 years. Pure-tone audiometry tests including high frequencies were performed to all individuals at one day before, same day and one month later with reference to the time of acoustic trauma. One day and four days after acoustic trauma, serum levels of vitamin B12, folic acid, zinc, magnesium and malondialdehyde were measured. RESULTS: After acoustic trauma, notch type hearing loss at 4000 Hz frequency was observed in 83 of the participants. However there was no significant difference among high frequency audiometry thresholds (p>0.05). There was a statistically significant difference between serum levels of malondialdehyde before and after acoustic t...
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.
A review on medicinal plants used for treating ototoxicity and acoustic trauma induced hearing loss
Brazilian Journal of Pharmaceutical Sciences, 2019
Hearing loss induced by chemotherapy and acoustic trauma is mainly associated with two factors, free radical formation and apoptosis pathway activation. Despite numerous efforts on reducing the effects of these factors, no definite strategy is still determined to interfere with and control these processes. In recent studies, various protective agents, including antioxidants have been used on animal models, to inhibit the formation of free radicals thus improving hearing loss.In this review article we will discuss the role of traditional herbal medicine in treatment of noise/drug induced hearing loss, focusing on medicinal plants' active substances,as well as their mechanisms of action in reducing or preventing the formation of free radicals thus increasing the rate of survival of cochlea cells. Data have been gathered since year 2000, from scientific publications including the following keywords: deafness, drug toxicity, acute trauma, medicinal herbs and oxidative stress. The study includes all herbs and medicinal plants that have been experimentally used in studies on animal models and clinical trials. The results from these studies indicate the effectiveness of most of these herbs and their active substances through their antioxidative properties. Medicinal plants reported in this review can thus be considered as effective remedies intreating noise/drug induced hearing loss,yet further studies need to be done.
Antioxidant treatment reduces blast-induced cochlear damage and hearing loss
Hearing Research, 2012
Exposure to blast overpressure has become one of the hazards of both military and civilian life in many parts of the world due to war and terrorist activity. Auditory damage is one of the primary sequela of blast trauma, affecting immediate situational awareness and causing permanent hearing loss. Protecting against blast exposure is limited by the inability to anticipate the timing of these exposures, particularly those caused by terrorists. Therefore a therapeutic regimen is desirable that is able to ameliorate auditory damage when administered after a blast exposure has occurred. The purpose of this study was to determine if administration of a combination of antioxidants 2,4-disulfonyl a-phenyl tertiary butyl nitrone (HPN-07) and N-acetylcysteine (NAC) beginning 1 h after blast exposure could reduce both temporary and permanent hearing loss. To this end, a blast simulator was developed and the operational conditions established for exposing rats to blast overpressures comparable to those encountered in an open-field blast of 14 pounds per square inch (psi). This blast model produced reproducible blast overpressures that resulted in physiological and physical damage to the auditory system that was proportional to the number and amplitude of the blasts. After exposure to 3 consecutive 14 psi blasts 100% of anesthetized rats had permanent hearing loss as determined at 21 days post exposure by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) testing. Animals treated with HPN-07 and NAC after blast exposure showed a significant reduction in ABR threshold shifts and DPOAE level shifts at 2e16 kHz with significant reduction in inner hair cell (IHC) and outer hair cell (OHC) loss across the 5e36 kHz region of the cochlea compared with control animals. The time course of changes in the auditory system was documented at 3 h, 24 h, 7 day and 21 day after blast exposure. At 3 h after blast exposure the auditory brainstem response (ABR) threshold shifts were elevated by 60 dB in both treated and control groups. A partial recovery of to 35 dB was observed at 24 h in the controls, indicative of a temporary threshold shift (TTS) and there was essentially no further recovery by 21 days representing a permanent threshold shift (PTS) of about 30 dB. Antioxidant treatment increased the amount of both TTS and PTS recovery relative to controls by 10 and 20 dB respectively. Distortion product otoacoustic emission (DPOAE) reached a maximum level shift of 25e30 dB measured in both control and treated groups at 3 h after blast exposure. These levels did not change by day 21 in the control group but in the treatment group the level shifts began to decline at 24 h until by day 21 they were 10e20 dB below that of the controls. Loss of cochlear hair cells measured at 21 day after blast exposure was mostly in the outer hair cells (OHC) and broadly distributed across the basilar membrane, consistent with the distribution of loss of frequency responses as measured by ABR and DPOAE analysis and typical of blast-induced damage. OHC loss progressively increased after blast exposure reaching an average loss of 32% in the control group and 10% in the treated group at 21 days. These findings provide the first evidence that a combination of antioxidants, HPN-07 and NAC, can both enhance TTS recovery and prevent PTS by reducing damage to the mechanical and neural components of the auditory system when administered shortly after blast exposure.