Eiju Kanagawa

Coenzyme Q10 Protects Hair Cells against Aminoglycoside

It is well known that the production of free radicals is associated with sensory cell death induced by an aminoglycoside. Many researchers have reported that antioxidant reagents protect sensory cells in the inner ear, and coenzyme Q10 (CoQ10) is an antioxidant that is consumed as a health food in many countries. The purpose of this study was to investigate the role of CoQ10 in mammalian vestibular hair cell death induced by aminoglycoside. Cultured utricles of CBA/CaN mice were divided into three groups (control group, neomycin group, and neomycin + CoQ10 group). In the neomycin group, utricles were cultured with neomycin (1 mM) to induce hair cell death. In the neomycin + CoQ10 group, utricles were cultured with neomycin and water-soluble CoQ10 (30–0.3 µM). Twenty-four hours after exposure to neomycin, the cultured tissues were fixed, and vestibular hair cells were labeled using an anti-calmodulin antibody. Significantly more hair cells survived in the neomycin + CoQ10 group than in the neomycin group. These data indicate that CoQ10 protects sensory hair cells against neomycin-induced death in the mammalian vestibular epithelium; therefore, CoQ10 may be useful as a protective drug in the inner ear.

A study of hearing function and histopathologic changes in the cochlea of the type 2 diabetes model Tsumura Suzuki obese diabetes mouse

Abstract Objectives: This study used Tsumura Suzuki Obese Diabetes (TSOD) mice as a spontaneous type 2 diabetes model and Tsumura Suzuki Non-obesity (TSNO) mice as controls to investigate factors involved in the onset of hearing impairment. Method: Body weight, blood glucose levels, and auditory brainstem responses (ABRs) were measured. The cochleae were excised and evaluated histopathologically. Results: The TSOD mice showed significant hyperglycemia at 2–7 months and severe obesity at 5–10 months; significantly elevated ABR thresholds at 8–10 months; and the capillary lumens in the cochlea stria vascularis were narrower in the TSOD mice than in the TSNO mice. At 17 months, India ink vascular staining of the TSOD mice’s cochleae revealed decreased capillary density in the stria vascularis. The vascular area of capillaries in the stria vascularis and the vascular area were significantly smaller in TSOD mice. Histopathological analysis showed vessel wall thickening in the modiolus and narrowed capillaries in the stria vascularis, suggesting reduced blood flow to the inner ear. Conclusion: The diabetes mice model used in our study showed early age-associated hearing loss, and histopathology showed findings of vessel wall thickening in the modiolus, narrowing of capillaries in the stria vascularis, and chronically reduced blood flow in the cochlea.

Effects of substance P during the recovery of hearing function after noise-induced hearing loss

Substance P (SP) is a widely distributed neurotransmitter in living tissues and is involved in various repair processes. We investigated the possibility that SP may ameliorate cochlear hair cell damage produced by noise exposure. The present study examined the effect of SP in protecting the cochlea from noise damage in guinea pigs exposed to noise after an infusion of SP into the inner ear. Changes in the hearing threshold (auditory brain response, ABR), number of synaptic ribbons, and the appearance of the outer hair cells after noise exposure were analyzed at 2 severity levels of noise-induced hearing loss. The moderate noise-induced hearing loss (110dB, 3h) group showed recovery in the ABR threshold over time, finally reaching a level slightly above pre-exposure levels, with only slight injury to the synaptic ribbons and minimal changes in the appearance of the outer hair cells. Our results indicated that in moderate hearing loss, SP exhibited a protective effect on the inner ear, both functionally and structurally. While the final magnitude of ABR threshold elevation was greater in severe noise-induced hearing loss, the synaptic ribbons and outer hair cells showed signs of severe damage.