The monitoring role of otoacoustic emissions and oxidative stress markers in the protective effects of antioxidant administration in noise-exposed subjects: a pilot study

摘要

Noise-induced hearing loss (NIHL) is a major cause of hearing disability, accounting for about 16 percent of all disabling hearing losses in the adult population worldwide (Nelson et al. 2005). Prevention of NIHL is based on several hearing-preservation methods, such as reduction of noise sources, the use of hearing-protection devices, the development of hearing-loss screening, and basic education for the high-risk population. In recent years, significant contributions to identify the underlying pathways of damage have been posted, with new perspectives for clinical prevention and treatment. Death of hair cells after acoustic trauma may be due to direct mechanical trauma and/or a result of increased metabolic activity in the inner ear (Le Prell et al. 2007). Several studies have shown that the generation of reactive oxygen species (ROS) and free radicals is involved in the cascade of cochlear events that induces acoustic trauma (Henderson et al. 2006). Depending on the severity, frequency, duration, and temporal characteristics of noise (impulse noise versus continuous noise), the effects on the cochlea range from a moderate disappearance of the hair cell stereocilia and moderate damage of the stria vascularis and lateral wall to a complete fracture of the organ of Corti and rupture of the Reissner's membrane (Hamernik et al. 1984). Evoked otoacoustic emissions (EOAEs) represent an accurate, objective, fast, and noninvasive tool for assessing outer hair cells (OHCs) function in experimental and clinical studies (Probst et al. 1991).