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

• mtDNA common deletion has a synergistic effect with chronic noise exposure in d-galactose-induced aging rats.
• mtDNA common deletion enhances noise-induced supporting cell damage in the organ of Corti.
• mtDNA common deletion increases noise-induced mitochondrial damage in the inner ear.
• mtDNA common deletion decreases the self-repairing capability within the cochlea after acoustic injury.

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.