Early elevation of cochlear reactive oxygen species following noise exposure

Reactive oxygen species (ROS) have been implicated in a growing number of neurological disease states, from acute traumatic injury to neurodegenerative conditions such as Alzheimer's disease. Considerable evidence suggests that ROS also mediate ototoxicant- and noise-induced cochlear injury, although most of this evidence is indirect. To obtain real-time assessment of noise-induced cochlear ROS production in vivo, we adapted a technique which uses the oxidation of salicylate to 2,3-dihydroxybenzoic acid as a probe for the generation of hydroxyl radical. In a companion paper we described the development and characterization of this method in cochlear ischemia-reperfusion. In the present paper we use this method to demonstrate early elevations in ROS production following acute noise exposure. C57BL/6J mice were exposed for 1 h to intense broad-band noise sufficient to cause permanent threshold shift (PTS), as verified by auditory brainstem responses. Comparison of noise-exposed animals with unexposed controls indicated that ROS levels increase nearly 4-fold in the period 1-2 h following exposure and do not decline over that time. Our ROS measures extend previous results indicating that noise-induced PTS is associated with elevated cochlear ROS production and ROS-mediated injury. Persistent cochlear ROS elevation following noise exposure suggests a sustained process of oxidative stress which might be amenable to intervention with chronic antioxidant therapy.