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The effect of intratympanic oxytocin treatment on rats exposed to acoustic trauma

Published online by Cambridge University Press:  17 May 2019

F C Akin Ocal ,
G G Kesici ,
S G Gurgen ,
R Ocal  and
S Erbek
F C Akin Ocal*
Affiliation:
Otorhinolaryngology Clinic, Gulhane Training and Research Hospital, Ankara, Turkey
G G Kesici
Affiliation:
Otorhinolaryngology Clinic, Ataturk Training and Research Hospital, Ankara, Turkey
S G Gurgen
Affiliation:
Department of Histology and Embryology, Celal Bayar University, Manisa, Turkey
R Ocal
Affiliation:
Otorhinolaryngology Clinic, Ataturk Training and Research Hospital, Ankara, Turkey
S Erbek
Affiliation:
Department of Otorhinolaryngology, Baskent University, Ankara, Turkey
*
Author for correspondence: Dr F Ceyda Akin Ocal, Otorhinolaryngology Clinic, Gulhane Training and Research Hospital, 38000 Ankara, Turkey E-mail: fceydaakin@gmail.com
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Abstract

Objective

To investigate whether oxytocin can prevent ototoxicity related to acoustic trauma.

Methods

Twenty-eight rats were divided into four groups: noise (group 1), control (group 2), noise plus oxytocin (group 3), and oxytocin (group 4). Intratympanic oxytocin was administered on days 1, 2, 4, 6, 8 and 10 in groups 3 and 4. Groups 1 and 3 were exposed to acoustic trauma. Distortion product otoacoustic emission and auditory brainstem response testing were performed in all groups.

Results

In group 1, auditory brainstem response thresholds increased significantly after acoustic trauma. In group 3, auditory brainstem response thresholds increased significantly on day 1 after acoustic trauma, but there were no significant differences between thresholds at baseline and on the 7th and 21st days. In group 1, significant differences were observed between distortion product otoacoustic emission signal-to-noise ratios measured before and on days 1, 7 and 21 after acoustic trauma. In group 3, no significant differences were observed between the distortion product otoacoustic emission signal-to-noise ratios measured before and on days 7 and 21 after acoustic trauma.

Conclusion

Oxytocin had a therapeutic effect on rats exposed to acoustic trauma in this experiment.

Keywords

Acoustic TraumaAuditory Brainstem ResponsesDistortion Product Otoacoustic EmissionHearing Loss

Information

Type
Main Articles
Information
The Journal of Laryngology & Otology , Volume 133 , Issue 6 , June 2019 , pp. 466 - 476
Copyright
Copyright © JLO (1984) Limited, 2019 

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Footnotes

Dr F C Akin Ocal takes responsibility for the integrity of the content of the paper

Presented at the ENT World Congress, 24–28 June 2017, Paris, France.

References

1Lim, HW, Choi, SH, Kang, HH, Ahn, JH, Chung, JW. Apoptotic pattern of cochlear outer hair cells and frequency-specific hearing threshold shift in noise-exposed BALB/c mice. Clin Exp Otorhinolaryngol 2008;1:80–5Google Scholar
2Bohne, BA, Harding, GW. Degeneration in the cochlea after noise damage: primary versus secondary events. Am J Otol 2000;21:505–9Google Scholar
3Mukherjea, D, Ghosh, S, Bhatta, P, Steth, S, Tupal, S, Borse, V et al. Early investigational drugs for hearing loss. Expert Opin Investig Drugs 2015;24:201–17Google Scholar
4Ohlemiller, KK, McFadden, SL, Ding, DL, Lear, PM, Ho, YS. Targeted mutation of the gene for cellular glutathione peroxidase (Gpx1) increases noise-induced hearing loss in mice. J Assoc Res Otolaryngol 2000;1:243–54Google Scholar
5Ohlemiller, KK, McFadden, SL, Ding, DL, Flood, DG, Reaume, AG, Hoffman, EK et al. Targeted deletion of the cytosolic Cu/Zn-superoxide dismutase gene (Sod1) increases susceptibility to noise-induced hearing loss. Audiol Neurootol 1999;4:237–46Google Scholar
6Le Prell, CG, Yamashita, D, Minami, SB, Yamasoba, T, Miller, JM. Mechanisms of noise-induced hearing loss indicate multiple methods of prevention. Hear Res 2007;226:22–43Google Scholar
7Ohinata, Y, Miller, JM, Altschuler, RA, Schacht, J. Intense noise induces formation of vasoactive lipid peroxidation products in the cochlea. Brain Res 2000;878:163–73Google Scholar
8Tuğtepe, H, Sener, G, Biyikli, NK, Yuksel, M, Cetinel, S, Gedik, N et al. The protective effect of oxytocin on renal ischemia/reperfusion injury in rats. Regul Pept 2007;140:101–8Google Scholar
9Dusunceli, F, Iseri, SO, Ercan, F, Gedik, N, Yegen, C, Yegen, BC. Oxytocin alleviates hepatic ischemia–reperfusion injury in rats. Peptides 2008;29:1216–22Google Scholar
10Elberry, AA, Refaie, SM, Kamel, M, Ali, T, Darwish, H, Ashourg, O. Oxytocin ameliorates cisplatin-induced nephrotoxicity in Wistar rats. Ann Saudi Med 2013;33:57–62Google Scholar
11Ramesh, G, Reeves, WB. p38 MAP kinase inhibition ameliorates cisplatin nephrotoxicity in mice. Am J Physiol Renal Physiol 2005;289:F166–74Google Scholar
12Tsuruya, K, Tokumoto, M, Ninomiya, T, Hirakawa, M, Masutani, K, Taniguchi, M et al. Antioxidant ameliorates cisplatin-induced renal tubular cell death through inhibition of death receptor-mediated pathways. Am J Physiol Renal Physiol 2003;285:F208–18Google Scholar
13Bıyıklı, NK, Tuğtepe, H, Şener, G, Velioğlu-Öğünç, A, Çetinel, Ş, Gedik, N et al. Oxytocin alleviates oxidative renal injury in pyelonephritic rats via a neutrophil-dependent mechanism. Peptides 2006;27:2249–57Google Scholar
14Iseri, SÖ, Şener, G, Sağlam, B, Gedik, N, Ercan, F, Yeğen, BC. Oxytocin protects against sepsis-induced multiple organ damage: role of neutrophils. J Surg Res 2005;126:73–81Google Scholar
15Rashed, LA, Hashem, RM, Soliman, HM. Oxytocin inhibits NADPH oxidase and P38 MAPK in cisplatin-induced nephrotoxicity. Biomed Pharmacother 2011;65:474–80Google Scholar
16Bekmez Bilmez, ZE, Aydin, S, Şanli, A, Altintoprak, N, Demir, MG, Atalay Erdoğan, B et al. Oxytocin as a protective agent in cisplatin-induced ototoxicity. Cancer Chemother Pharmacol 2016;77:875–9Google Scholar
17Hu, BH, Henderson, D, Nicotera, TM. Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise. Hear Res 2002;166:62–71Google Scholar
18Van Campen, LE, Murphy, WJ, Franks, JR, Mathias, PI, Toraason, MA. Oxidative DNA damage is associated with intense noise exposure in the rat. Hear Res 2002;164:29–38Google Scholar
19Miller, JM, Brown, JN, Schacht, J. 8-iso-prostaglandin F(2alpha), a product of noise exposure, reduces inner ear blood flow. Audiol Neurootol 2003;8:207–21Google Scholar
20Kurioka, T, Matsunobu, T, Niwa, K, Tamura, A, Satoh, Y, Shiotani, A. Activated protein C rescues the cochlea from noise-induced hearing loss. Brain Res 2014;1583:201–10Google Scholar
21Aksoy, F, Dogan, R, Yenigun, A, Veyseller, B, Ozturan, O, Ozturk, B. Thymoquinone treatment for inner-ear acoustic trauma in rats. J Laryngol Otol 2015;129:38–45Google Scholar
22Salt, AN, Plontke, SK. Local inner-ear drug delivery and pharmacokinetics. Drug Discov Today 2005;10:1299–306Google Scholar
23Wang, X, Dellamary, L, Fernandez, R, Harrop, A, Keithley, EM, Harris, JP et al. Dose-dependent sustained release of dexamethasone in inner ear cochlear fluids using a novel local delivery approach. Audiol Neurootol 2009;14:393–401Google Scholar
24Yamane, H, Nakai, Y, Takayama, M, Iqucgi, H, Nakaqawa, T, Kojima, A. Appearance of free radicals in the guinea pig inner ear after noise-induced acoustic trauma. Eur Arch Otorhinolaryngol 1995;252:504–8Google Scholar
25Henderson, D, Bielefeld, EC, Harris, KC, Hu, BH. The role of oxidative stress in noise-induced hearing loss. Ear Hear 2006;27:1–19Google Scholar
26Davis, B, Qiu, W, Hamernik, R. Sensitivity of distortion product otoacoustic emissions in noise-exposed chinchillas. J Am Acad Audiol 2005;16:69–78Google Scholar