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Year : 2018  |  Volume : 10  |  Issue : 2  |  Page : 60-64

Prestin, otolin-1 regulation, and human 8-oxoG DNA glycosylase 1 gene polymorphisms in noise-induced hearing loss

1 Department of Biochemistry, Faculty of Medicine, Assiut University, Assiut, Egypt
2 Department of Otolaryngology, Faculty of Medicine, Banha University, Banha, Egypt

Correspondence Address:
Dr. Randa Samir Hana
Department of Biochemistry, Faculty of Medicine, Assiut University, Assiut
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijmbs.ijmbs_4_18

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Background: Noise induces free radicals release and can damage the cochlear epithelium. The outer hair cell motor protein prestin is necessary for sharp frequency tuning and cochlear function. Otolin-1 is a glycoprotein; its mRNA expression is restricted to the inner ear. Genes involved in repairing the oxidative damage as human 8-oxoG DNA glycosylase 1 (hOGG1) can affect the cochlea susceptibility to noise. Prestin upregulation may represent a response to compensate for noise-induced hearing loss (NIHL). Objectives: We investigated the association between exposure to noise, the blood perstin and otolin-1level, hOGG1 polymorphisms, and oxidative DNA damage as indicated by serum 8-hydroxy-2'-deoxyguanosine (8-OHdG) concentrations. Materials and Methods: In 300 patients with NIHL and 200 controls with normal hearing, blood prestin, otolin-1, and 8-OHdG levels were studied by ELISA; the hOGG1 polymorphism was genotyped by polymerase chain reaction amplification followed by digestion with restriction endonucleases. Results: The prestin, otolin-1, and 8-OHdG levels were significantly elevated in patients compared to controls (P < 0.05). Regression analysis showed that hOGG1 Cys/Cys genotype showed a significantly increased risk of hearing loss compared with the other genotypes exposed to the same environmental factors (95% confidence interval = 1.1–2.3, adjusted odds ratio = 1.5). This was associated with increased prestin, otolin-1, and 8-OHdG levels and the duration of noise exposure in months. Conclusion: These findings are consistent with the notion that prestin increases in an attempt to compensate for missing outer hair cells. Otolin-1 could be a circulatory biomarker for otoconia damage caused by noise, and the hOGG1 Cys/Cys genotype could be a susceptibility marker for NIHL. The hOGG1 Cys/Cys gene variant was more frequent in patients compared to controls exposed to the same environmental factors and more frequent in severe cases confirmed by elevated prestin, otolin-1, and 8-OHdG l levels.

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