scholarly journals The Protective Effect of Intratympanic Dexamethasone on Streptomycin Ototoxicity in Rats

2017 ◽  
Vol 96 (6) ◽  
pp. E12-E17 ◽  
Author(s):  
Aylin Göl ◽  
Engin Şengül ◽  
Beyhan Yılmaz ◽  
Fazıl Emre Özkurt ◽  
Mehmet Akdağ ◽  
...  

The purpose of this experimental study was to investigate the protective role of intratympanically administered dexamethasone on the inner ears of rats that were exposed to streptomycin ototoxicity. Twenty-four adult Wistar albino rats were separated into 4 groups: Group 1 (only streptomycin), Group 2 (only intratympanic dexamethasone), Group 3 (streptomycin and intratympanic dexamethasone), and Group 4 (streptomycin and intratympanic saline). All rats were evaluated with distortion product otoacoustic emissions (DPOAE) tests before the start of treatment and on the day it ended. On the 45th day, after the final DPOAE tests, animals of all groups were sacrificed under general anesthesia. The differences between the amplitudes of DPOAE results were determined, and hearing results were statistically analyzed. Also, the cochleas of each rat were histopathologically evaluated under a light microscope with hematoxylin and eosin staining. In the intratympanic dexamethasone group it was observed that cochlear hair cells were mostly protected. No significant difference was seen between the DPOAE results before and after treatment (p > 0.05). On the other hand, loss was observed in the hearing functions and hair cells of the rats that received streptomycin and streptomycin plus intratympanic saline (p < 0.05). In the streptomycin plus intratympanic dexamethasone group, the cochlear hair cells were partially protected. A significant difference was observed when the DPOAE results (DP-grams) of the streptomycin plus intratypmanic dexamethasone group were compared to those of the streptomycin plus intratympanic saline group (p < 0.05). After the experimental study, ototoxic effects of the administration of streptomycin and intratympanic dexamethasone were observed on the rats’ cochlear hair cells. We conclude that intratympanic dexamethasone has protective effects against this cochlear damage in rats.

Author(s):  
Swetapadma Nayak ◽  
Rajeshwary Aroor ◽  
Usha Shastri ◽  
M. K. Goutham ◽  
Devika Sinha

Abstract Objective The prolonged exposure to electromagnetic fields of mobile phones can damage the cochlear hair cells, which can be detected by otoacoustic emission (OAE). To know the effect of mobile phones on hearing, the young volunteers were subjected to prolonged mobile phone usage and changes in OAE were recorded. Materials and Methods Twenty-eight volunteers with normal hearing were made to talk one full hour continuously on the mobile phone. Distortion product otoacoustic emission (DPOAE) was measured prior to the usage of mobile phones and immediately after the use (post-exposure 1) and 24 hours after the use (post-exposure 2). The values were compared. Results Out of the 28 volunteers, 20 were females and 8 were males. Twenty-one volunteers preferred the right ear while using mobile phones, 7 preferred the left ear. There was no statistically significant difference between the baseline DPOAE values and values of post-exposure 1 and 2 when only the preferred ear was taken into consideration. When the preferred ear was compared with nonpreferred ear, a statistically significant difference was found only in the low frequencies between the pre-exposure and post-exposure 1 values. Conclusion This study shows there was no significant correlation between OAE and prolonged mobile phone exposure when the preferred ear was not considered.


2010 ◽  
Vol 125 (4) ◽  
pp. 348-353 ◽  
Author(s):  
G Kayabasoglu ◽  
O S Sezen ◽  
G Eraslan ◽  
E Aydin ◽  
T Coskuner ◽  
...  

AbstractObjective:To study the effects of the electromagnetic field emitted by cellular telephones upon the inner ear of rats, using distortion product otoacoustic emissions.Methods:Forty Wistar Albino rats were used. Twenty newborn and 20 adult rats were divided into two groups of 10, one to participate in the study and one as a control. The rats were exposed to the electromagnetic field for 6 hours per day, for 30 consecutive days. Before and after the 30 day exposure period, distortion product otoacoustic emissions were measured in each group and a signal-to-noise ratio calculated, which was later used in statistical analysis.Results:For both the newborn and adult rat groups, there was no significant difference in distortion product otoacoustic emissions recorded before and after exposure to the cellular telephone electromagnetic field (p > 0.05).Conclusion:Exposure to the electromagnetic field emitted by cellular telephones, for 6 hours a day for 30 consecutive days, had no effect on the hearing of newborn or adult rats, at the outer ear, middle ear or cochlear level.


2017 ◽  
Vol 22 (04) ◽  
pp. 364-367 ◽  
Author(s):  
Prashanth Prabhu ◽  
Akhila Chandrashekhar ◽  
Janani Cariappa ◽  
Nayanika Ghosh

Introduction Individuals with blood group O are reported to have reduced otoacoustic emissions (OAEs) compared with individuals with different blood groups. Objective The present study attempted to determine if the blood group has any effect on high-frequency auditory sensitivity using ultrahigh-frequency audiometry and ultrahigh-frequency distortion product otoacoustic emissions (DPOAEs). Methods High-frequency thresholds and high-frequency DPOAEs were measured in 60 individuals with normal hearing and different blood groups. Results The results of the study showed that there was a significant reduction in DPOAE amplitude for individuals with blood group O compared with individuals with other blood groups. However, there was no significant difference in ultrahigh-frequency thresholds across the blood groups. Conclusion This reduction in OAE amplitude may be attributed to a lower number of healthy outer hair cells in individuals with blood group O. Further studies on larger groups of individuals are essential for a better generalization of the results.


2013 ◽  
Vol 40 (2) ◽  
Author(s):  
Asti Kristianti ◽  
Teti Madiadipoera ◽  
Bogi Soeseno

Background: Chemotherapy is worldwide used nowadays, and its toxicity still remain a problemespecially toxicity to the ear (ototoxicity). Cisplatin (cis-diamminedichloroplatinum) is one of themost commonly used chemotherapy and highly potent in treating epithelial malignancies. Ototoxicitycaused by cisplatin is irreversible, progressive, bilateral, sensorineural hearing loss especially on highfrequency (4-8 KHz) accompanied by tinnitus. Purpose: To observe the cochlear outer hair cells damagein malignancies patients treated with cisplatin. Methods: This study is an observational analytic studywith prospective design to determine the influence of high dose cisplatin on cochlear outer hair cellsfunction. The research was carried out at the ENT-HNS Department, Hasan Sadikin General HospitalBandung, from November 2007 until June 2008. Audiometry, tympanometry, and distortion productotoacoustic emission (DPOAE) examinations were conducted before chemotherapy and DPOAE, andtimpanometry was again measured three days after first and second cycles of cisplatin administration. McNemar test was performed to calculate the effects of high-dose cisplatin to the cochlear outer haircells function. To compare pre and post-cisplatin on alteration of cochlear hair cells function, Wilcoxontest was used. Results: In this study 60 ears from 30 subjects that meet the inclusion criteria, consistedof 25 man (83.3%) and 5 women (16.7%). The prevalence of damaged cochlear outer hair cells were63% at first cycle and 70% at second cycle of cisplatin administration. The decline of cochlear outerhair cells function was significant (p<0.001). Conclusion: High-dose cisplatin decreases cochlear outerhair cells function in patients with malignant neoplasm. Abstrak : Latar belakang: Kemoterapi sekarang rutin digunakan secara klinis di seluruh dunia. Sejalan denganhal tersebut toksisitas kemoterapi, khususnya terhadap telinga saat ini menjadi perhatian. Sisplatin(cis-diamminedichloroplatinum) adalah salah satu obat kemoterapi yang paling banyak digunakandan paling manjur untuk terapi keganasan epitelial. Efek ototoksik sisplatin yaitu terjadi gangguandengar sensorineural yang irreversible, progresif, bilateral pada frekuensi tinggi (4-8 kHz), dan disertaidengan tinitus. Tujuan: Untuk menilai penurunan fungsi sel rambut luar koklea pada penderita tumorganas sesudah pemberian sisplatin dosis tinggi dengan menggunakan DPOAE. Metode: Studi analitikobservasional dengan rancangan prospektif di Bagian IK. THT-KL RS. Hasan Sadikin Bandung mulaibulan November 2007 sampai dengan Juni 2008. Pada penelitian ini dilakukan pemeriksaan audiometrinada murni, timpanometri, dan distortion product otoacoustic emission (DPOAE) prakemoterapi, kemudianDPOAE dan timpanometri diulang tiga hari sesudah siklus pertama dan kedua kemoterapi sisplatin. Datayang diperoleh diuji dengan uji McNemar dan uji Wilcoxon. Hasil: Dari penelitian didapat 60 telingadari 30 subjek penelitian yang memenuhi kriteria inklusi yang terdiri dari 25 laki-laki (83,3%) dan 5perempuan (16,7%). Insidens penurunan fungsi sel rambut luar koklea sebesar 63% (38 kasus) sesudahsiklus pertama dan 70% (42 kasus) sesudah siklus kedua. Hubungan penurunan fungsi sel rambut luarkoklea memberikan nilai yang sangat bermakna sejak pemberian siklus pertama (p<0,001). Kesimpulan:Pemberian sisplatin dosis tinggi pada penderita tumor ganas menyebabkan penurunan fungsi sel rambutluar koklea.Kata kunci: kemoterapi, sisplatin dosis tinggi, sel rambut luar koklea.


2021 ◽  
pp. 014556132199018
Author(s):  
Murat Koc ◽  
Abdullah Dalgic ◽  
Mehmet Ziya Ozuer

Objective: To investigate the effects of the mechanical trauma to the round window, a model electrode inserted into the scala tympani on the cochlear reserve, and the efficacy of topical steroids in preventing hearing loss. Materials and Methods: 21 male Wistar Albino rats were equally categorized into three groups. In all groups an initial mechanical injury to round window was created. Only subsequent dexamethasone injection was administrated into the cochlea in the subjects of group 2 while a multichannel cochlear implant guide inserted into the cochlea prior to dexamethasone administration for group 3. Distortion product otoacoustic emissions (DPOAEs) were obtained prior to and immediately after the surgical injury, eventually on postoperative seventh day (d 7). Mean signal/noise ratios (S/Ns) obtained at 2000, 3000, and 4000 Hz were calculated. Data sets were compared with non-parametric statistical tests. Results: The early intraoperative mean S/Ns were significantly less than preoperative measurements for group 1 and 2; however, preoperative and postoperative d 7 average S/Ns did not differ. There was statistically significant difference between preoperative, intraoperative and postoperative d 7 average S/Ns for group 3. Conclusion: We observed that hearing was restored approximately to the preoperative levels following early postoperative repair. However, an electrode insertion into the cochlea via round window subsequent to mechanical trauma seems to cause a progressive hearing loss. Therefore, a special care must be taken to avoid the injury to the round window membrane in the course of the placement of a cochlear implant electrode and surgery for the chronic otitis media.


2018 ◽  
Vol 47 (2) ◽  
pp. 102
Author(s):  
Meyrna Heryaning Putri ◽  
Pudji Rahaju ◽  
Dyah Indrasworo

Latar belakang: Kemoterapi neoadjuvan adalah induksi kemoterapi sebelum radioterapi dengan regimen cisplatin dan 5-Fluorouracil. Kemoterapi cisplatin bersifat ototoksik pada pendengaran sensorineural bilateral progresif dan bersifat irreversible. Kriteria dari American Speech-Language Hearing Association (ASHA) dan Common Terminology Criteria for Adverse Events (CTCAE) merupakan kriteria untuk mengidentifikasi ototoksisitas dengan menggunakan audiometri, selain pemeriksaan Distortion Product Otoacoustic Emissions (DPOAE). Tujuan: Mengidentifikasi hubungan ototoksisitas dengan kemoterapi neoadjuvan pada penderita karsinoma nasofaring (KNF) WHO tipe III menggunakan ASHA, CTCAE, serta DPOAE. Metode: Studi ini adalah penelitian observasional dengan desain cohort. Kriteria inklusi penelitian yaitu penderita baru KNF WHO tipe III, yang mendapatkan kemoterapi regimen standar dan berusia <60 tahun. Kriteria pemeriksaan DPOAE adalah penderita dengan ambang dengar ≤40 dB. Percontoh dilakukan pemeriksaan timpanometri, audiometri, dan DPOAE. Hasil: Terdapat 9 sampel percontoh penelitian. Uji repeated-ANOVA menunjukkan tidak ditemukan perbedaan bermakna pada tiga hasil pengukuran audiometri antara pascakemoterapi pertama, kedua, dan ketiga (p>0,05). Deteksi awal ototoksisitas menggunakan kriteria ASHA menunjukkan sensitivitas sebesar 67% dan dan CTCAE 44%, dibandingkan baku emas menggunakan DPOAE. Kesimpulan: Ototoksisitas cisplatin ditemukan sejak kemoterapi pertama dengan menggunakan pemeriksaan DPOAE walaupun tidak bermakna secara statistik. Kemampuan DPOAE untuk mendeteksi awal ototoksisitas lebih baik dibandingkan kriteria ASHA dan CTCAE yang menggunakan audiometri nada murni.Kata kunci: Karsinoma nasofaring, ototoksisitas sisplatin, DPOAE, CTCAE, ASHA ABSTRACT Introduction: Neoadjuvant chemotherapy is induction chemotherapy before radiotherapy with cisplatin and 5-Fluorouracyl regiment. Chemotherapy cisplatin is ototoxic, leads to frequently progresive and irreversible bilateral sensorineural hearing loss. American Speech-Language Hearing Association (ASHA) and Common Terminology Criteria for Adverse Events (CTCAE) are the criteria to determine ototoxicity with audiometry, beside Distortion Product Otoacoustic Emissions (DPOAE). Purpose: To identify the relationship between ototoxicity with neoadjuvant chemotherapy in patients NPC WHO type III using ASHA, CTCAE, and DPOAE. Method: This observational study approach with cohort design. Inclusion criteria: new patients NPC WHO type III who consented to undergo standard regiment chemotherapy, and age <60 year-old. For DPOAE examination: hearing level ≤40 dB. Exclucion criteria: NPC WHO type III patients who underwent chemotherapy with unconventional standard regiment. Examinations for hearing function conducted with tympanometry, pure tone audiometry, and Distortion Product Otoacoustic Emissions (DPOAE). Result: There were 9 sample in this study. The result of Repeated-ANOVA test showed no significant difference in three audiometry measurements among three series of chemotherapies. Early detection of ototoxicity using ASHA and CTCAE criterias showed sensitivity of 67% and 44% (compared with DPOAE as a gold standard). Conclusion: Cisplatin ototoxicity had occured since the first chemotherapy and detected with DPOAE, but statistically was not significantly related. Early detection of cisplatin ototoxicity with DPOAE was much better than with criteria American Speech-Language Hearing Association (ASHA) and Common Terminology Criteria for Adverse Events (CTCAE), which used pure tone audiometry.Keywords: Nasopharyngeal carcinoma, cisplatin ototoxicity, DPOAE, CTCAE, ASHA


2007 ◽  
Vol 97 (4) ◽  
pp. 2930-2936 ◽  
Author(s):  
Stéphane F. Maison ◽  
Lisan L. Parker ◽  
Lucy Young ◽  
John P. Adelman ◽  
Jian Zuo ◽  
...  

Cochlear hair cells express SK2, a small-conductance Ca2+-activated K+ channel thought to act in concert with Ca2+-permeable nicotinic acetylcholine receptors (nAChRs) α9 and α10 in mediating suppressive effects of the olivocochlear efferent innervation. To probe the in vivo role of SK2 channels in hearing, we examined gene expression, cochlear function, efferent suppression, and noise vulnerability in mice overexpressing SK2 channels. Cochlear thresholds, as measured by auditory brain stem responses and otoacoustic emissions, were normal in overexpressers as was overall cochlear morphology and the size, number, and distribution of efferent terminals on outer hair cells. Cochlear expression levels of SK2 channels were elevated eightfold without striking changes in other SK channels or in the α9/α10 nAChRs. Shock-evoked efferent suppression of cochlear responses was significantly enhanced in overexpresser mice as seen previously in α9 overexpresser mice; however, in contrast to α9 overexpressers, SK2 overexpressers were not protected from acoustic injury. Results suggest that efferent-mediated cochlear protection is mediated by other downstream effects of ACh-mediated Ca2+ entry different from those involving SK2-mediated hyperpolarization and the associated reduction in outer hair cell electromotility.


2017 ◽  
Vol 119 ◽  
pp. 26-39 ◽  
Author(s):  
Kohei Yamahara ◽  
Takayuki Nakagawa ◽  
Juichi Ito ◽  
Kazuo Kinoshita ◽  
Koichi Omori ◽  
...  

2004 ◽  
Vol 20 (6-10) ◽  
pp. 141-147 ◽  
Author(s):  
Alpaslan Terzi ◽  
Mustafa Iraz ◽  
Semsettin Sahin ◽  
Atilla Ilhan ◽  
Nuri Idiz ◽  
...  

Rotenone, an insecticide of botanical origin, causes toxicity through inhibition of complex I of the respiratory chain in mitochondria. This study was undertaken to determine whether rotenone-induced liver oxidant injury is prevented by erdosteine, a mucolytic agent showing antioxidant properties. There were four groups of Male Wistar Albino rats: group one was untreated as control; the other groups were treated with erdosteine (50 mg/kg per day, orally), rotenone (2.5 mg/mL once and 1 mL/kg per day for 60 days, i.p.) or rotenone plus erdosteine, respectively. Rotenone treatment without erdosteine increased xanthine oxidase (XO) enzyme activity and also increased lipid peroxidation in liver tissue P < 0.05). The rats treated with rotenone plus erdosteine produced a significant decrease in lipid peroxidation and XO activities in comparison with rotenone group PB / 0.05). Erdosteine treatment with rotenone led to an increase in catalase (CAT) and superoxide dismutase (SOD) activities in comparison with the rotenone group PB / 0.05). There was no significant difference in nitric oxide (NO) level between groups. There were negative correlations between CAT activity and malondialdehyde (MDA) level (r= -0.934, P <0.05) with between CAT and SOD activities (r= -0.714, P <0.05), and a positive correlation between SOD activity and MDA level (r= 0.828, P <0.05) in rotenone group. In the rotenone plus erdosteine group, there was a negative correlation between XO activity and NO level in liver tissue (r= -0.833, P -0.05). In the light of these findings, erdosteine may be a protective agent for rotenone-induced liver oxidative injury in rats.


2007 ◽  
Vol 26 (6) ◽  
pp. 519-525 ◽  
Author(s):  
A. Gokcimen ◽  
A. Cim ◽  
H.T. Tola ◽  
D. Bayram ◽  
A. Kocak ◽  
...  

The aim of this study was to compare the possible protective effects of N-acetylcysteine (NAC), caffeic acid (CAPE) and vitamin E (Vit-E) on doxorubicin-induced hepatotoxicity. Thirty-two male Wistar albino rats, weighing between 250 and 350 g were supplied and randomly divided into five groups. Animals in study groups were pretreated with a single dose of doxorubicin (Dox), which was administered intraperitoneally (i.p.). Control group (Group I) was treated with intraperitoneal saline injection. Group II did not received any antioxidant agent after the injection. Group III and Group IV were given CAPE and intraperitoneal vitamin E injection for eight days, respectively. Group V received NAC for eight days. The study was finished after 10 days. Tissue samples were collected from all animals and histopathological examination was performed. There was statistically significant difference between the experiment groups and controls by means of mononuclear cell infiltration and diameters of hepatic sinusoid, terminal hepatic venule (central vein) and portal area (portal canal). Changes related with hepatocellular damage were more prominent, whereas there was no significant difference between Dox and NAC given groups histopathologically. It was observed that structural changes were regressed after CAPE administration. However, this recovery was more prominent in vitamin E given group. These findings suggest that Dox induced liver damage could be efficiently reversed by vitamin E administration. It has been found that CAPE, but not NAC has protective effects on Dox-induced hepatocellular damage. Human & Experimental Toxicology (2007) 26, 519—525


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