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

被引:112
作者
Tavanai, Elham [1 ]
Mohammadkhani, Ghassem [1 ]
机构
[1] Univ Tehran Med Sci, Sch Rehabil, Dept Audiol, Enghelab Ave, Tehran, Iran
关键词
Age-related hearing loss; Presbycusis; Oxidative stress; mtDNA deletion; Antioxidant therapy; BRAIN-STEM RESPONSES; MITOCHONDRIAL-DNA; OXIDATIVE STRESS; INNER-EAR; RADICAL SCAVENGERS; DIETARY RESTRICTION; COMMON DELETION; VITAMIN INTAKE; C57BL/6J MICE; MOUSE MODELS;
D O I
10.1007/s00405-016-4378-6
中图分类号
R76 [耳鼻咽喉科学];
学科分类号
100213 ;
摘要
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 ELSE VIER, 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.
引用
收藏
页码:1821 / 1834
页数:14
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