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Review
. 2017 Apr;274(4):1821-1834.
doi: 10.1007/s00405-016-4378-6. Epub 2016 Nov 17.

Role of antioxidants in prevention of age-related hearing loss: a review of literature

Affiliations
Review

Role of antioxidants in prevention of age-related hearing loss: a review of literature

Elham Tavanai et al. Eur Arch Otorhinolaryngol. 2017 Apr.

Abstract

Age-related hearing loss (ARHL), also known as presbycusis, is one of the most prevalent chronic degenerative conditions. It is characterized by a decline in auditory function. ARHL is caused by the interaction of multiple factors, including cochlear aging, environment, genetic predisposition, and health comorbidities. The primary pathology of ARHL includes the hair cells loss, stria vascularis atrophy, and loss of spiral ganglion neurons as well as the changes in central auditory pathways. The research to date suggests that oxidative stress and mitochondrial DNA deletion (mtDNA) play a major role in pathophysiology of ARHL. Therefore, similar to other otological conditions, several studies have also showed that antioxidants can slow ARHL, but some also indicate that antioxidant therapy is not a magic elixir that will prevent or treat hearing loss associated with aging completely, but why? All available clinical trials, including animal and human studies, in English language that examined the protective effects of antioxidants against ARHL were reviewed. Materials were obtained by searching ELSEVIER, PubMed, Scopus, Web of knowledge, Google Scholar databases, Clinical trials, and Cochrane database of systematic reviews. Although ARHL has been shown to be slowed by supplementation with antioxidants, particularly in laboratory animals, a few studies have investigated the effect of interventions against ARHL in humans. High-quality clinical trials are needed to investigate if ARHL can be delayed or prevented in humans. However, it seems that targeting several cell-death pathways is better than targeting the only oxidative stress pathway.

Keywords: Age-related hearing loss; Antioxidant therapy; Oxidative stress; Presbycusis; mtDNA deletion.

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