Oxidative Stresses and Mitochondrial Dysfunction in Age-Related Hearing Loss

• Published in: Oxidative medicine and cellular longevity Vol. 2014; no. 2014; pp. 1 - 6
• Main Authors: Fujimoto, Chisato, Yamasoba, Tatsuya
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01-01-2014; John Wiley & Sons, Inc
• Subjects: Aging; Animals; Antioxidants - metabolism; Antioxidants - therapeutic use; Caloric Restriction; Cellular control mechanisms; Cochlear Nerve - physiopathology; Development and progression; DNA Damage; DNA, Mitochondrial - chemistry; DNA, Mitochondrial - genetics; DNA, Mitochondrial - metabolism; Health aspects; Hearing loss; Hearing Loss - metabolism; Hearing Loss - pathology; Hearing Loss - prevention & control; Humans; Mitochondria - genetics; Mitochondria - metabolism; Oxidative Stress; Reactive Oxygen Species - metabolism; Review
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2014/582849

Age-related hearing loss (ARHL), the progressive loss of hearing associated with aging, is the most common sensory disorder in the elderly population. The pathology of ARHL includes the hair cells of the organ of Corti, stria vascularis, and afferent spiral ganglion neurons as well as the central auditory pathways. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Mitochondria play a crucial role in the induction of intrinsic apoptosis in cochlear cells. ARHL can be prevented in laboratory animals by certain interventions, such as caloric restriction and supplementation with antioxidants. In this review, we will focus on previous research concerning the role of the oxidative stress and mitochondrial dysfunction in the pathology of ARHL in both animal models and humans and introduce concepts that have recently emerged regarding the mechanisms of the development of ARHL.