Yin Shankai, Yu Zhiping, Sockalingam Ravi, Bance Manohar, Sun Genlou, Wang Jian
Institute of Otolaryngology Research, JiaoTong University, Shanghai, 200233, China.
Neurobiol Dis. 2007 Sep;27(3):370-7. doi: 10.1016/j.nbd.2007.06.006. Epub 2007 Jun 13.
Age-related hearing loss, or presbycusis, has been associated with large-scale mitochondrial DNA (mtDNA) deletion in previous studies. However, the role of this mtDNA damage in presbycusis is still not clear because the deletion in inner ears has not been measured quantitatively and analyzed in parallel with the time course of presbycusis. In the present study, the deletion was quantified using quantitative real-time PCR (qRT-PCR) in male Fischer 344 rats of different ages. It was found that the deletion increased quickly during young adulthood and reached over 60% at 6 months of age. However, a significant hearing loss was not seen until after 12 months of age. The results suggest that the existence of the deletion per se does not necessarily imply cochlear damage, but rather a critical level of the accumulated deletion seems to precede the hearing loss. The long delay may indicate the involvement of mechanisms other than mtDNA deletion in the development of presbycusis.
在先前的研究中，年龄相关性听力损失（即老年性聋）已与大规模线粒体DNA（mtDNA）缺失相关联。然而，这种mtDNA损伤在老年性聋中的作用仍不明确，因为内耳中的缺失尚未进行定量测量，也未与老年性聋的病程进行平行分析。在本研究中，使用定量实时PCR（qRT-PCR）对不同年龄的雄性Fischer 344大鼠的缺失进行了定量。结果发现，缺失在成年早期迅速增加，在6个月大时达到60%以上。然而，直到12个月大后才出现明显的听力损失。结果表明，缺失本身的存在并不一定意味着耳蜗损伤，而是累积缺失的临界水平似乎先于听力损失出现。这种长时间的延迟可能表明在老年性聋的发生发展中，除了mtDNA缺失之外，还有其他机制的参与。
