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We investigated whether the oxidoreductase cofactor pyrroloquinoline quinone (PQQ) prevents noise-induced and age-related hearing loss (NIHL and ARHL) in mice. To assess NIHL, 8 week-old mice with and without PQQ administration were exposed to noise for 4 h. PQQ was orally administered for one week before and after noise exposure and subcutaneously once before noise exposure. For ARHL evaluation, mice were given drinking water with or without PQQ starting at 2 months of age. In the NIHL model, PQQ-treated mice had auditory brainstem response (ABR) thresholds of significantly reduced elevation at 8 kHz, a significantly increased number of hair cells at the basal turn, and significantly better maintained synapses beneath the inner hair cells compared to controls. In the ARHL model, PQQ significantly attenuated the age-related increase in ABR thresholds at 8 and 32 kHz at 10 months of age compared to controls. In addition, the hair cells, spiral ganglion cells, ribbon synapses, stria vascularis and nerve fibers were all significantly better maintained in PQQ-treated animals compared to controls at 10 months of age. These physiological and histological results demonstrate that PQQ protects the auditory system from NIHL and ARHL in mice.

Ameliorating effect of noisy galvanic vestibular stimulation (nGVS) on posture varies among subjects. In this feasibility study, we investigated the association between original postural instability and the ameliorating effect of nGVS on posture. Data were collected in a previously published study. Thirty healthy elderly were recruited. Two nGVS sessions (30 min or 3 h) were performed in a randomised order. The optimal intensity of nGVS, the most effective intensity for improving posture, was determined before each session. Posture was measured for 30 s during and after nGVS in the eyes-closed/foam rubber condition. The velocity, envelopment area, and root mean square of the centre of pressure movement without nGVS were significantly larger in the group with an optimal intensity than those in the group without an optimal intensity. There was a significant positive correlation between these values and the long-term ameliorating effects. The ratio of the values in the eyes-closed/foam rubber condition to those in the eyes-open condition was significantly larger in the group with an optimal intensity, and had a significant correlation with the long-term ameliorating effects. The ameliorating effects are greater in subjects who were originally unstable and in those whose postural stability was relatively independent of vestibular input.

We aimed at determining the mitochondrial function in premature senescence model of auditory cells. Short exposure to H2O2 (1 h, 0.1 mM) induced premature cellular senescence in House Ear Institute-Organ of Corti 1 auditory cells. The transmission electron microscopy analysis revealed that damaged mitochondria and autophagosomes containing dense organelles appeared in the auditory cells after short exposure to H2O2. The branch and junction parameters of the skeletonized image of the mitochondria were found to decrease significantly in H2O2-treated cells. A branched reticulum of tubules was poorly formed, featuring coexistence of numerous tiny clusters along with few relatively large entities in the H2O2-treated cells. In terms of bioenergetics, H2O2-treatment led to the dose-dependent decrease in mitochondrial membrane potential in the auditory cells. The fragmented mitochondria (fusion fission) was slightly lower than the control cells. The short-time exposure of live auditory cells to H2O2 damaged the mitochondrial respiratory capacity without any effect on the baseline ATP production rates. The vulnerability of the mitochondrial membrane potential to the uncoupling reagent was increased after H2O2 treatment. Our findings indicated that the mitochondrial dysfunction due to the decline in the O2 consumption rate should be the first event of premature senescence process in the auditory cells, resulting in the imbalance of mitochondrial fusion/fission and the collapse of the mitochondrial network., Auditory system senescence: Mitochondrial dynamics and respiration The mitochondrial morphology and physiology could influence the process of age-related hearing loss. Prof. Tatsuya Yamasoba’s research group at the University of Tokyo has examined the functional changes of mitochondria in terms of its respiratory function, membrane potential and morphology under premature senescence induced by oxidative stress in an auditory cell line. The morphological and functional mitochondrial damage were observed as the respiratory capacity deficiency and the fluctuation of the fusion/fission balance. Their results provide evidence of the fundamental interdependence between mitochondrial metabolic activity and its network structure in premature senescence process of auditory cells. This is a pioneer study to indicate the influence of mitochondrial dynamics and respiratory system on the premature senescence process of auditory cells. Further studies into inter cellular communication including cytoskeleton and nucleus can help us understand the etiology underlying age-related hearing loss.