Noise-induced hearing loss: treatment and prevention

Noise-induced hearing loss (NIHL) is one of the most common sensory disabilities in humans. NIHL is ranked as the world's top industrial injury and a significant cause of hearing loss in teenagers, thus affecting many age groups. This research is timely since a recent study has demonstrated that NIHL has increased dramatically in adolescents, with a 30% increase in this group in the past 10 years, thus coining the term “MP3” generation. The implications of the "MP3" generation will lead to increasing long-term health costs and life-long hearing problems necessitating the use of hearing aids from a young age. Research has shown that exposure to acoustic trauma causes an increase in metabolic activity within the inner ear, with a initial peak in free radical production during the acoustic trauma (within hours) followed by a secondary peak at seven to 10 days after the trauma. Free radicals cause decreased cochlear blood flow, excitotoxic neuronal swelling, and induction of cell death within the inner ear. Recent studies have demonstrated that antioxidant treatments can scavenge free radicals and thus attenuate downstream effects of free radical production. While this has been a major breakthrough for NIHL research, the specific roles played by the different classes of free radicals (reactive nitrogen/oxygen species) remains unclear. The aims of this project were: AIM 1: To determine whether inhibition of reactive nitrogen species can prevent NIHL, using taurine as a nitric oxide scavenger. AIM 2: To establish if there was a dose-dependant response to any effect observed. The research directly addresses a prominent and recognised otolaryngological disease that affects mental and social health. The long-term goal is to develop a pharmaceutical therapy for NIHL to ultimately prevent a debilitating disease and improve human health. Our work also looks at early use of stem cell therapies to repair after acoustic trauma.