The role of mitochondrial oxidative stress in hearing loss

Abstract

Hearing loss is the most common form of sensory impairment in humans, affecting 5.3% worldwide population. Although approximately 1 in 500 children are born with impaired hearing, sudden or progressive forms of hearing loss can manifest at any age. Hearing impairment following cochlear damage due to noise trauma, ototoxicity or age‐related cochlear degeneration was linked to a common pathogenesis involving the formation of reactive oxygen species (ROS). This review summarizes the current data suggesting a role of mitochondrial ROS overproduction in hearing loss and the molecular mechanism involved in hair cell apoptosis responsible of this disorder. Because increasing number of studies demonstrated that antioxidants and free radical scavengers may serve as effective compounds to block the activation of cochlear hair cell death, targeting members of antioxidant pathways and in the breakdown of superoxide anions and hydrogen peroxidase, could be feasible options for the treatment of several types of hearing loss.