Dai Pu, Yang Weiyan, Jiang Sichang, Gu Rui, Yuan Huijun, Han Dongyi, Guo Weiwei, Cao Juyang
Department of Otolaryngology-Head and Neck Surgery, Chinese PLA General Hospital, Beijing, People's Republic of China.
Acta Otolaryngol. 2004 Mar;124(2):130-6. doi: 10.1080/00016480410016586.
To study the relationships between cochlear hypoxia, mitochondrial (mt) DNA4977 deletion and metabolic features of mtDNA in presbyacusis.
Sixty-seven temporal bones from a presbyacusis group, an age-matched control group and a young and middle-aged control group were involved in the experiment. Nested and tri-nested polymerase chain reactions (PCRs) were applied to test for the presence of the mtDNA4977 deletion. Computer imaging processing was used to measure blood vessel parameters in the internal acoustic meatus (IAM).
The mtDNA4977 deletion was detected in 17/34 ears in the presbyacusis group, 4/19 ears in the age-matched control group and 0/14 ears in the young and middle-aged control group. In the presbyacusis group, the lumen of the vasa nervorum of the IAM showed a more severe narrowing in cases with than without the mtDNA4977 deletion.
The high incidence of the mtDNA4977 deletion in the temporal bones of presbyacusis patients suggests a correlation between the mtDNA4977 deletion and presbyacusis. Hypoxia of the cochlea may cause the mtDNA4977 deletion and other mtDNA mutants and furthermore may cause a reduction in mitochondrial oxidative phosphorylation and decreased function of the acoustic neural system. The symptoms of presbyacusis may occur when the function of the acoustic neural system is impaired as a result of abnormal mtDNA metabolism reaching a particular threshold.
研究老年性聋中耳蜗缺氧、线粒体(mt)DNA4977缺失与mtDNA代谢特征之间的关系。
将老年性聋组、年龄匹配对照组以及中青年对照组的67块颞骨纳入实验。采用巢式和三重巢式聚合酶链反应(PCR)检测mtDNA4977缺失的存在情况。运用计算机图像处理技术测量内耳道(IAM)血管参数。
老年性聋组34耳中有17耳检测到mtDNA4977缺失,年龄匹配对照组19耳中有4耳检测到,中青年对照组14耳中未检测到。在老年性聋组中,存在mtDNA4977缺失的病例,其IAM神经血管的管腔狭窄比无该缺失的病例更严重。
老年性聋患者颞骨中mtDNA4977缺失的高发生率表明mtDNA4977缺失与老年性聋之间存在相关性。耳蜗缺氧可能导致mtDNA4977缺失及其他mtDNA突变,进而可能导致线粒体氧化磷酸化减少以及听神经系统功能下降。当mtDNA代谢异常达到特定阈值导致听神经系统功能受损时,可能会出现老年性聋症状。