Mitochondrial DNA common deletion increases susceptibility to noise-induced hearing loss in a mimetic aging rat model

Noise-induced hearing loss (NIHL) is an important occupational health hazard. However, susceptibility to NIHL remains poorly understood. The present study was designed to investigate whether mitochondrial DNA common deletion (CD) increases the susceptibility of individuals to NIHL. A mimetic aging r...

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Bibliographic Details
Published in:	Biochemical and biophysical research communications 2014-10, Vol.453 (3), p.515-520
Main Authors:	Yu, Jintao, Wang, Yanjun, Liu, Peng, Li, Qingyu, Sun, Yu, Kong, Weijia
Format:	Article
Language:	eng
Subjects:	Aging - physiology Animals DNA, Mitochondrial - genetics Female Genetic Predisposition to Disease Hearing Loss - genetics Models, Animal Noise - adverse effects Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction Sequence Deletion
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Summary:	Noise-induced hearing loss (NIHL) is an important occupational health hazard. However, susceptibility to NIHL remains poorly understood. The present study was designed to investigate whether mitochondrial DNA common deletion (CD) increases the susceptibility of individuals to NIHL. A mimetic aging rat model harboring increased CD in the inner ear was established by chronic d-galactose administration, and the synergic effect of CD and noise on hearing sensitivity was assessed. We determined that although developed the same magnitude of temporary threshold shifts and hair cell loss, the d-galactose treated rats with increased CD in the inner ear exhibited a longer hearing recovery process and experienced higher permanent hearing threshold shifts at high frequencies than the saline-treated control rats. Greater supporting cell damage and stria vascularis ultrastructural changes were observed in d-galactose treated rats three weeks after recovery. The results suggested that the elevated CD in the inner ear could increase an individual's susceptibility to NIHL, which likely through a reduction in the self-repairing capability within the cochlea after acoustic injury.
ISSN:	0006-291X 1090-2104