The role of oxidative stress in noise-induced hearing loss

Abstract

Modern research has provided new insights into the biological mechanisms of noise-induced hearing loss, and with these new insights comes hope for possible prevention or treatment. Underlying the classic set of cochlear pathologies that occur as a result of noise exposure are increased levels of reactive oxygen species (ROS) that play a significant role in noise-induced hair cell death. Both necrotic and apoptotic cell death have been identified in the cochlea. Included in the current review is a brief review of ROS, along with a description of sources of cochlear ROS generation and how ROS can damage cochlear tissue. The pathways of necrotic and apoptotic cell death are also reviewed. Interventions are discussed that target the prevention of noise-induced hair cell death: the use of antioxidants to scavenge and eliminate the damaging ROS, pharmacological interventions to limit the damage resulting from ROS, and new techniques aimed at interrupting the apoptotic biochemical cascade that results in the death of irreplaceable hair cells.