山东大学耳鼻喉眼学报 ›› 2014, Vol. 28 ›› Issue (4): 95-99.doi: 10.6040/j.issn.1673-3770.0.2013.308

• 综述 • 上一篇    下一篇

mtDNACD4977与老年性聋相关性的研究进展

刘红1, 王帅2, 王海波1   

  1. 1. 山东大学附属省立医院 耳鼻咽喉头颈外科, 山东 济南 250021;
    2. 山东大学附属省立医院 胸外科, 山东 济南 250021
  • 收稿日期:2013-11-04 出版日期:2014-08-16 发布日期:2014-08-16
  • 通讯作者: 王海波。Email：whbotologic797@163.com E-mail:whbotologic797@163.com
  • 作者简介:刘红。Email：halaye@aliyun.com
  • 基金资助:
    山东省科技发展计划（2012G0021838）；国家重点基础研究发展计划（2014CB541703）

Review on mtDNACD4977 and presbyacusis

LIU Hong1, WANG Shuai2, WANG Hai-bo1   

  1. 1. Department of Otolaryngology & Head and Neck Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China;
    2. Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China
  • Received:2013-11-04 Online:2014-08-16 Published:2014-08-16

PDF (PC)

551

摘要： 半个世纪以来，老年性聋发病率在全球范围内持续增长。据美国公共卫生署统计，75岁以上的老年人约40%～66%的有听力损失，而超过80岁的老年人80%以上有听力损失[1-3]。老年性聋是随着年龄逐步进展，双耳对称性的，以感音神经性为主的慢性进行性听力减退，又称年龄相关的听力损失[4-6]。它是年龄增长后听觉器官逐步衰老的过程，是听觉系统精细结构处理信息发生障碍的过程[7]。老年性聋是由多种危险因子的长期累积损害而成，其中年龄是最重要的危险因子。而长期慢性疾病，如高血压、糖尿病能引起内耳供血的减少，也会进一步加重听力的损害[1，8-9]。随着生物医学的不断发展，许多学者发现老年性聋患者不仅伴有核基因组的改变，线粒体DNA（mitochondrial DNA，mtDNA）的突变和缺失在老年性聋的发生、发展过程中也发挥重要作用[2，6，10]。

关键词: 老年性聋, 自由基, 氧化损伤, 线粒体DNA 4977 bp

Abstract: Since half a century ago, the incidence of presbycusis grows worldwide. Based on the data from United States Public Health Service (PHS), hearing loss affects approximately 40%～66% of adults age 75 and older. Among them, more than 80% were older than 85 years old[1-3]. Presbycusis, also called age-related hearing loss, is a chronic, progressive, bilateral, symmetrical and sensorineural hearing loss[4-6]. It's a pregressive aging of auditory organs, which involves in the disorders of fine-structure in auditory system dealing with information[7]. Presbycusis is caused by long-term cumulative damage under a variety of risk factors. Age is the most important risk factor. Chronic diseases, such as diabetes and hypertension, could also cause blood supply decrease in inner ear, which further leads to the hearing damages[1,8-9]. With the development of biomedicine, many scholars have found that alternation of nuclear genome, mutation and deletion of mitochondrial DNA play significant roles in the onset and development of presbycusis[2,6,10].

Key words: Mitochondrial DNA 4977 bp, Presbyacusis, Free radical, Oxidative stress

中图分类号: 

  • R764.43
[1] Mao Z, Zhao L, Pu L, et al. How well can centenarians hear?[J]. PLoS One, 2013, 8(6):e65565.
[2] Yamasoba T, Someya S, Yamada C, et al. Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss[J]. Hear Res, 2007, 226(1-2):185-193.
[3] Sprinzl G M, Riechelmann H. Current trends in treating hearing loss in elderly people: a review of the technology and treatment options-a mini-review[J]. Gerontology, 2010, 56(3):351-358.
[4] Bared A, Ouyang X, Angeli S, et al. Antioxidant enzymes, presbycusis, and ethnic variability[J]. Otolaryngol Head Neck Surg, 2010, 143(2):263-268.
[5] 胡岢.老年性耳聋的研究进展[J].中国听力语言康复科学杂志, 2005, 9(11):8-11.
[6] Yamasoba T, Lin F R, Someya S, et al. Current concepts in age-related hearing loss: epidemiology and mechanistic pathways[J]. Hear Res, 2013, 303:30-38.
[7] 王硕.感音神经性听力损失对患者使用时域包络与精细结构信息感知言语的影响[J].中华耳鼻咽喉头颈外科杂志, 2013, 48(2):171-174.
[8] Lasisi A O, Abiona T, Gureje O. The prevalence and correlates of self-reported hearing impairment in the Ibadan study of ageing[J]. Trans R Soc Trop Med Hyg, 2010, 104(8):518-523.
[9] Niu R, Yoshida M, Ling F. Increases in mitochondrial DNA content and 4977-bp deletion upon ATM/Chk2 checkpoint activation in HeLa cells[J]. PLoS One, 2012, 7(7):e40572.
[10] Dai P, Yang W, Jiang S, et al. Correlation of cochlear blood supply with mitochondrial DNA common deletion in presbyacusis[J]. Acta Otolaryngol, 2004, 124(2):130-136.
[11] Sequeira A, Martin M V, Rollins B, et al. Mitochondrial mutations and polymorphisms in psychiatric disorders[J]. Front Genet, 2012, 3:103.
[12] Malik A N, Czajka A. Is mitochondrial DNA content a potential biomarker of mitochondrial dysfunction?[J]. Mitochondrion, 2013, 13(5):481-492.
[13] Lagouge M, Larsson N G. The role of mitochondrial DNA mutations and free radicals in disease and ageing[J]. J Intern Med, 2013, 273(6):529-543.
[14] Zhong Y, Hu Y J, Yang Y, et al. Contribution of common deletion to total deletion burden in mitochondrial DNA from inner ear of d-galactose-induced aging rats[J]. Mutat Res, 2011, 712(1-2):11-19.
[15] Chen B, Zhong Y, Peng W, et al. Age-related changes in the central auditory system: comparison of D-galactose-induced aging rats and naturally aging rats[J]. Brain Res, 2010, 1344:43-53.
[16] 孔维佳, 胡钰娟, 王琼, 等.大鼠内耳拟老化伴线粒体突变模型的建立[J].临床耳鼻咽喉科杂志, 2006, 20(19):888-893.
[17] Kim E J, Kim S Y, Yun H J, et al. Detection and quantification of a radiation-associated mitochondrial DNA deletion by a nested real-time PCR in human peripheral lymphocytes[J]. Mutat Res, 2012, 749(1-2):53-59.
[18] Gendron S P, Mallet J D, Bastien N, et al. Mitochondrial DNA common deletion in the human eye: a relation with corneal aging[J]. Mech Ageing Dev, 2012, 133(2-3):68-74.
[19] Zhang X, Han D, Ding D, et al. Deletions are easy detectable in cochlear mitochondrial DNA of Cu/Zn superoxide dismutase gene knockout mice[J]. Chin Med J (Engl), 2002, 115(2):258-263.
[20] Kong W J, Hu Y J, Wang Q, et al. The effect of the mtDNA4834 deletion on hearing[J]. Biochem Biophys Res Commun, 2006, 344(1):425-430.
[21] Wang B, Van Veldhoven P P, Brees C, et al. Mitochondria are targets for peroxisome-derived oxidative stress in cultured mammalian cells[J]. Free Radic Biol Med, 2013, 65C:882-894.
[22] Yamasoba T, Someya S, Yamada C, et al. Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss[J]. HearRes, 2007, 226(1-2):185-193.
[23] Markaryan A, Nelson E G, Hinojosa R. Quantification of the mitochondrial DNA common deletion in presbycusis[J]. Laryngoscope, 2009, 119(6):1184-1189.
[24] 韩维举, 韩东一, 姜泗长, 等.人听觉器官线粒体DNA4977缺失与老年聋的关系[J].中华耳鼻咽喉科杂志, 2000, 35(6):416-419.
[25] Youle R J, Narendra D P. Mechanisms of mitophagy[J]. Nat Rev Mol Cell Biol, 2011, 12(1):9-14.
[26] Tengan C H, Gabbai A A, Shanske S, et al. Oxidative phosphorylation dysfunction does not increase the rate of accumulation of age-related mtDNA deletions in skeletal muscle[J]. Mutat Res, 1997, 379(1):1-11.
[27] Mendelev N, Mehta S L, Witherspoon S, et al. Upregulation of human selenoprotein H in murine hippocampal neuronal cells promotes mitochondrial biogenesis and functional performance[J]. Mitochondrion, 2011, 11(1):76-82.
[28] Zhao X Y, Sun J L, Hu Y J, et al. The effect of overexpression of PGC-1αon the mtDNA 4834 common deletion in a rat cochlear marginal cell senescence model[J]. Hear Res, 2013, 296(1):13-24.
[29] Ameur A, Stewart J B, Freyer C, et al. Ultra-deep sequencing of mouse mitochondrial DNA: mutational patterns[J]. PLoS Genet, 2011, 7(3):e1002028.
[30] Long J D, Matson W R, Juhl A R, et al.PREDICT-HD Investigators and Coordinators of the Huntington Study Group. 8OHdG as a marker for Huntington disease progression[J]. Neurobiol Dis, 2012, 46(3):625-634.
[31] Seidman M D. Effects of dietary restriction and antioxidants on presbyacusis[J]. Laryngoscope, 2000, 110(5 Pt 1):727-738.
[1] 许明,罗兴谷,唐洪波,江青山. 儿童突发性聋的临床特征及预后相关因素分析[J]. 山东大学耳鼻喉眼学报, 2018, 32(5): 41-44.
[2] 陈伟,胡中南,童钊君,李湘宇,刘文君. 青中年无眩晕、心脑血管疾病病史的突发性聋患者高刺激率听性脑干反应特征分析[J]. 山东大学耳鼻喉眼学报, 2018, 32(5): 45-49.
[3] 朱文燕,金新,佘万东,马永驰. 突发性聋30例精神心理状况分析[J]. 山东大学耳鼻喉眼学报, 2018, 32(5): 50-52.
[4] 黄芳,郑智娟,谢磊. 突发性聋患者焦虑、抑郁与病情阶段的关系及影响因素分析[J]. 山东大学耳鼻喉眼学报, 2018, 32(4): 1-6.
[5] 宋峰,甘彬,许安廷,王坚. 长时程低强度噪声暴露对豚鼠内毛细胞带状突触的影响分析[J]. 山东大学耳鼻喉眼学报, 2017, 31(5): 41-44.
[6] 张玉波,岳丽艳,尹晓妍,吕哲,单春光. 耳鸣治疗仪联合银杏叶提取物注射液治疗突聋伴耳鸣的疗效分析[J]. 山东大学耳鼻喉眼学报, 2017, 31(5): 50-53.
[7] 张转,刘涛,白治丽,周长明. 氧化应激与噪音性聋发病机制及治疗进展[J]. 山东大学耳鼻喉眼学报, 2017, 31(5): 101-103.
[8] 董健菲,陆玲,杨烨,高下. 合并脑白质异常聋儿人工耳蜗植入后听力言语及认知能力评估分析[J]. 山东大学耳鼻喉眼学报, 2017, 31(2): 43-48.
[9] 马荣峰,朱富高,孙美红,付涛,张晓恒,曹琳. 突发性聋预后的相关因素分析及疗程选择[J]. 山东大学耳鼻喉眼学报, 2016, 30(4): 69-74.
[10] 孙昌志, 刘文龙, 李琰, 罗仁忠. 双耳感音神经性聋患儿合并分泌性中耳炎的临床诊治[J]. 山东大学耳鼻喉眼学报, 2015, 29(4): 11-14.
[11] 钟晓声, 杨海弟, 郑亿庆. 突发性聋伴耳鸣患者耳鸣特征[J]. 山东大学耳鼻喉眼学报, 2015, 29(4): 15-18.
[12] 卢娜. 三种不同给药途径治疗突发性感音神经性耳聋的效果对比[J]. 山东大学耳鼻喉眼学报, 2015, 29(2): 24-27.
[13] 张彩霞, 刘阳云, 陈志喜, 江文, 李正贤, 陈琼, 常恩格. 鼓室激素注射为初始治疗的突发性聋听力恢复的时间规律[J]. 山东大学耳鼻喉眼学报, 2015, 29(1): 15-18.
[14] 卢振东1，杨军2. 听觉剥夺和耳蜗内电刺激引起幼鼠听觉通路bdnf和c-fos基因及蛋白改变[J]. 山东大学耳鼻喉眼学报, 2012, 26(3): 17-23.
[15] 梁志成，覃冠锻，莫炼. 特发性突聋伴眩晕对患者预后的影响[J]. 山东大学耳鼻喉眼学报, 2012, 26(2): 42-43.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
No Suggested Reading articles found!
网站版权所有 © 2018 《山东大学耳鼻喉眼学报》编辑部　
地址：山东省济南市山大南路27号（250100）电话：+86-0531-88366912 E-mail: ebhxb@sdu.edu.cn
本系统由北京玛格泰克科技发展有限公司设计开发