Abstract

Noise is one of the most common causes of hearing loss in industrial countries. There are many studies about chemical agents to prevent noise-induced hearing loss (NIHL). However, there is no commercially available drug yet. Retinoic acid is an active metabolite of Vitamin A; it has an anti-apoptic role in NIHL. This study aims to verify the differences among selective agonists of retinoic acid receptors (RARs) in NIHL. All-trans retinoic acid (ATRA), AM80 (selective retinoic acid receptor α agonist), AC261066 (Selective retinoic acid receptor β1 agonist), and CD1530 (Selective retinoic acid λ agonist) were injected to 6–7 weeks old CJ5BL/6 mice before noise (110 dB for 3 h) exposure. In the auditory brainstem response test pre-, post 1, 3, and 7 days after noise exposure, not only ATRA but all kinds of selective RAR agonists showed protective effects in hearing threshold and wave I amplitude. Though there was no significant difference in the level of protective effects between agonists, α agonist showed the most prominent effect in preserving hearing function as well as outer hair cells after noise exposure. In conclusion, selective agonists of RAR demonstrate comparable protective effects against NIHL to retinoic acid. Given that these selective RAR agonists have less side effects than retinoic acid, they may be promising potential drugs against NIHL.

Highlights

  • Noise-induced hearing loss (NIHL) is a common form of hearing loss inin industrial countries.In particular, enhanced exposure to noise in work places can result in hearing loss

  • The outer hair cells of the cochlea are highly vulnerable to noise exposure

  • We examined the effect of selective administration of retinoic acid receptors (RARs) agonists to prevent NIHL

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Summary

Introduction

Noise-induced hearing loss (NIHL) is a common form of hearing loss inin industrial countries. Enhanced exposure to noise in work places can result in hearing loss. The number of patients with NIHL has greatly increased, making it a significant public health problem. Organization estimates that 1.1 billion young people worldwide could be at risk of hearing loss [1]. The mechanisms of NIHL comprise both direct mechanical damage and metabolic damage. Excessive noise can cause damage to middle ear structures, round and oval window membranes, and the organ of Corti. The outer hair cells of the cochlea are highly vulnerable to noise exposure. Noise can distort the stereocilia of hair cells, causing defects in mechanotransduction. Free radicals (e.g., reactive oxygen species) can damage the cell membrane through necrosis or apoptosis of neighboring cells [2]

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