Noise-Induced Hearing Loss: The Potential for Otoprotection

Abstract

Noise-induced hearing loss (NIHL) is a significant clinical, social, and economic issue. Although we once thought virtually all NIHL was a consequence of mechanical damage to cells in the inner ear, we now know that intense metabolic activity drives the formation of free radicals (short-lived, unstable, highly reactive clusters of atoms) in the inner ear. Studies in animals clearly have shown that free radicals formed during and after noise contribute importantly to NIHL, and many laboratories have demonstrated that free radical scavengers (“antioxidants”) reduce NIHL in animal subjects. Our group, including investigators at multiple institutions, specifically has shown the combination of beta-carotene, vitamins C and E, and magnesium is highly effective in preventing NIHL and sensory cell death in guinea pigs and mice. Others have shown benefit in animal models with agents such as N-acytelcysteine, D-methionine, and ebselen. Use of free radical scavengers or antioxidants to prevent noise-induced deficits thus has become a clinical research goal. Given the multitude of intracellular events that occur during and after noise, it is possible that combinations of agents will ultimately prove to be a useful therapeutic approach. Translational investigations are essential to confirm potential utility of these agents in the human inner ear.