Early elevation of cochlear reactive oxygen species following noise exposure

Reactive oxygen species (ROS) have been implicated in a growing number of n eurological disease states, from acute traumatic injury to neurodegenerativ e conditions such as Alzheimer's disease. Considerable evidence suggests th at ROS also mediate ototoxicant- and noise-induced cochlear injury, althoug h most of this evidence is indirect. To obtain real-time assessment of nois e-induced cochlear ROS production in vivo, we adapted a technique which use s the oxidation of salicylate to 2,3-dihydroxybenzoic acid as a probe for t he generation of hydroxyl radical. In a companion paper we described the de velopment and characterization of this method in cochlear ischemia-reperfus ion. in the present paper we use this method to demonstrate early elevation s in ROS production following acute noise exposure. C57BL/6J mice were expo sed for 1 h to intense broad-band noise sufficient to cause permanent thres hold shift (PTS), as verified by auditory brainstem responses. Comparison o f noise-exposed animals with unexposed controls indicated that ROS levels i ncrease nearly 4-fold in the period 1-2 h following exposure and do not dec line over that time. Our ROS measures extend previous results indicating th at noise-induced PTS is associated with elevated cochlear ROS production an d ROS-mediated injury. Persistent cochlear ROS elevation following noise ex posure suggests a sustained process of oxidative stress which might be amen able to intervention with chronic antioxidant therapy.