Cellular and molecular mechanisms involved in age-related hearing loss with focusing on oxidative stress

Document Type : Review Paper

Authors

1 Department of Medical Researches, Cicilav Medical Facilities, Brayati, Erbil, Iraq

2 Department of Basic Sciences, College of Medicine, Hawler Medical University, Erbil, Iraq

Abstract

Age-related hearing loss (ARHL) is a type of bilateral hearing loss that progresses from low frequencies to high frequencies with age. This disorder is classified as a multifactorial disease. Factors involved in ARHL pathology are divided into two categories of genetic and non-genetic factors. The genes involved in this disorder include three categories of genes involved in cochlear structure and function, genes correlated with oxidative stress, and mitochondrial-dependent genes. Oxidative stress, apoptosis, and inflammation are the three main causes of ARHL. Damage to hair cells induces intrinsic and extrinsic apoptosis and can therefore accelerate ARHL. Some process in cells leads to the production of high amounts of reactive oxygen species including hydrogen peroxide (H2O2), anion superoxide (O2-), and hydroxyl radical (OH). Reactive oxygen species or ROS can generally have several sources including nitric oxide synthase, NADPH oxidase, microsomal, mitochondrial, and proxisomal pathways. In typical conditions, ROS is produced and neutralized by antioxidant enzymes such as superoxide dismutase, catalase, and glutathione, balancing cell homeostasis. Though, the process of aging, drug treatment, and some other factors upset this homeostasis, and this causes oxidative stress and induction of ARHL in the cells of the auditory system. The aim of this study was to describe the cellular and molecular mechanisms involved in ARHL with a focus on oxidative stress.

Graphical Abstract

Cellular and molecular mechanisms involved in age-related hearing loss with focusing on oxidative stress

Highlights

  • ARHL is characterized by increasing age and hearing loss from low to high frequencies.
  • Factors involved in ARHL are divided into two genetic and non-genetic categories.
  • Inflammation, apoptosis, and oxidative stress are three main mechanisms of ARHL.

Keywords

Main Subjects


1. Bowl MR, Dawson SJ. Age-related hearing loss. Cold Spring Harbor Perspect Med 2019; 9(8): a033217.
2. Yazdi AK, Davoudi-Dehaghani E, Anari MR, Fouladi P, Ebrahimi E, Sabeghi S, Eftekharian A, Fatemi KS, Emami H, Sharifi Z, Ramezanzadeh F. The first successful application of preimplantation genetic diagnosis for hearing loss in Iran. Cell Mol Biol 2018; 64(9).
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
3. Ciorba A, Bianchini C, Pelucchi S, Pastore A. The impact of hearing loss on the quality of life of elderly adults. Clin Interv Age 2012; 7: 159.
4. Tawfik KO, Klepper K, Saliba J, Friedman RA. Advances in understanding of presbycusis. J Neurosci Res 2020; 98(9): 1685-1697.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
5. Azeez SH, Jafar SN, Aziziaram Z, Fang L, Mawlood AH, Ercisli MF. Insulin-producing cells from bone marrow stem cells versus injectable insulin for the treatment of rats with type I diabetes. Cell Mol Biomed Rep 2021; 1(1): 42-51.
6. Bowl MR, Dawson SJ. The mouse as a model for age-related hearing loss-a mini-review. Gerontology 2015; 61(2): 149-157.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
7. Liu XZ, Yan D. Ageing and hearing loss. J Pathol J Pathol Soc Great Br Ireland 2007; 211(2): 188-197.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
8. Kamogashira T, Fujimoto C, Yamasoba T. Reactive oxygen species, apoptosis, and mitochondrial dysfunction in hearing loss. BioMed Res Int 2015; 2015.
9. Riva C, Donadieu E, Magnan J, Lavieille JP. Age-related hearing loss in CD/1 mice is associated to ROS formation and HIF target proteins up-regulation in the cochlea. Exp Gerontol 2007; 42(4): 327-336.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
10. Fujimoto C, Yamasoba T. Oxidative stresses and mitochondrial dysfunction in age-related hearing loss. Oxidative medicine and cellular longevity. 2014; 2014.
12. Chen H, Tang J. The role of mitochondria in age-related hearing loss. Biogerontology 2014; 15(1): 13-19.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
13. Tadros SF, D’Souza M, Zhu X, Frisina RD. Apoptosis-related genes change their expression with age and hearing loss in the mouse cochlea. Apoptosis 2008; 13(11): 1303-1321.
14. Someya S, Prolla TA. Mitochondrial oxidative damage and apoptosis in age-related hearing loss. Mech Age Dev 2010; 131(7-8): 480-486.
15. Someya S, Xu J, Kondo K, Ding D, Salvi RJ, Yamasoba T, Rabinovitch PS, Weindruch R, Leeuwenburgh C, Tanokura M, Prolla TA. Age-related hearing loss in C57BL/6J mice is mediated by Bak-dependent mitochondrial apoptosis. Proc Nat Acad Sci 2009; 106(46): 19432-19437.
16. Nolan LS, Cadge BA, Gomez-Dorado M, Dawson SJ. A functional and genetic analysis of SOD2 promoter variants and their contribution to age-related hearing loss. Mech Age Dev 2013; 134(7-8): 298-306.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
17. Watson N, Ding B, Zhu X, Frisina RD. Chronic inflammation–inflammaging–in the ageing cochlea: a novel target for future presbycusis therapy. Age Res Rev 2017; 40: 142-148.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
18. Kalinec GM, Lomberk G, Urrutia RA, Kalinec F. Resolution of cochlear inflammation: novel target for preventing or ameliorating drug-, noise-and age-related hearing loss. Front Cell Neurosci 2017; 11: 192.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
20. Wang J, Puel JL. Presbycusis: an update on cochlear mechanisms and therapies. J Clin Med 2020; 9(1): 218.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
21. Falah M, Najafi M, Houshmand M, Farhadi M. Expression levels of the BAK1 and BCL2 genes highlight the role of apoptosis in age-related hearing impairment. Clin Interv Age 2016; 11: 1003.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
22. Roth TN. Aging of the auditory system. Handbook Clin Neurol 2015; 129: 357-373.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed       
23. Wiwatpanit T, Remis NN, Ahmad A, Zhou Y, Clancy JC, Cheatham MA, García-Añoveros J. Codeficiency of lysosomal mucolipins 3 and 1 in cochlear hair cells diminishes outer hair cell longevity and accelerates age-related hearing loss. J Neurosci 2018; 38(13): 3177-3189.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
24. Manche SK, Jangala M, Putta P, Koralla RM, Akka J. Association of oxidative stress gene polymorphisms with presbycusis. Gene 2016; 593(2): 277-283.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
25. Gonzalez-Gonzalez S. The role of mitochondrial oxidative stress in hearing loss. Neurol Disord Ther 2017; 1: 1-5.
26. Tavanai E, Mohammadkhani G. Role of antioxidants in prevention of age-related hearing loss: a review of literature. Eur Arch Oto Rhino Laryngol 2017; 274(4): 1821-1834.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
27. Wong AC, Ryan AF. Mechanisms of sensorineural cell damage, death and survival in the cochlea. Front Age Neurosci 2015; 7: 58.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed       
29. Wang J, Puel JL. Toward cochlear therapies. Physiol Rev 2018; 98(4): 2477-2522.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed       
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
31. Rabinowitz PM, Wise Sr JP, Mobo BH, Antonucci PG, Powell C, Slade M. Antioxidant status and hearing function in noise-exposed workers. Hear Res 2002; 173(1-2): 164-171.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed   
32. Ding M, Duan X, Feng X, Wang P, Wang W. Application of CRS‐PCR‐RFLP to identify CYP1A1 gene polymorphism. J Clin Lab Anal 2017; 31(6): e22149.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
33. Zeng FG. Trends in cochlear implants. Trends Amplific 2004; 8(1): 1-34.
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed    PubMed Central   
34. Chang P. Implantable hearing devices: beyond hearing aids. Aust Fam Physician 2005; 34(3).
CrossRef    Google Scholar    full-text PDF    Mendeley    PubMed       
35. Ercisli MF, Lechun G, Azeez SH, Hamasalih RM, Song S, Aziziaram Z. Relevance of genetic polymorphisms of the human cytochrome P450 3A4 in rivaroxaban-treated patients. Cell Mol Biomed Rep 2021; 1(1): 33-41.
36. Aziziaram Z, Bilal I, Zhong Y, Mahmod AK, Roshandel MR. Protective effects of curcumin against naproxen-induced mitochondrial dysfunction in rat kidney tissue. Cell Mol Biomed Rep 2021; 1(1): 23-32.
37. Wen L, Zhang Y, Yang B, Han F, Ebadi AG, Toughani M. Knockdown of Angiopoietin-like protein 4 suppresses the development of colorectal cancer. Cell Mol Biol 2020; 66(5): 117-124.
38. Yang M, Abdalrahman H, Sonia U, Mohammed A, Vestine U, Wang M, Ebadi AG, Toughani M. The application of DNA molecular markers in the study of Codonopsis species genetic variation, a review. Cell Mol Biol 2020; 2: 23-30.
39. Bao S, Ebadi A, Toughani M, Dalle J, Maseleno A, Yıldızbası A. A new method for optimal parameters identification of a PEMFC using an improved version of Monarch Butterfly Optimization Algorithm. Int J Hydrogen Energy 2020; 45(35): 17882-17892.