Early Elevation of Cochlear Reactive Oxygen Species following Noise Exposure

TLDR

Reactive oxygen species are implicated in neurological disorders and are increasingly recognized as mediators of noise‑induced cochlear injury. To obtain real‑time assessment of noise‑induced cochlear ROS production in vivo, we adapted a salicylate‑based probe that detects hydroxyl radicals. C57BL/6J mice were exposed to 1 h of intense broadband noise that caused permanent threshold shift, and ROS production was measured by oxidation of salicylate to 2,3‑dihydroxybenzoic acid. ROS levels rose nearly fourfold within 1–2 h after exposure and remained elevated, indicating sustained oxidative stress that may be targeted by chronic antioxidant therapy.

Abstract

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.