Abstract

The hearing loss from exposure to noise and ototoxic drugs share a number of audiological and pathological similarities. Recent research has shown that reactive oxygen species (ROS) may be a common factor in both noise- and drug-induced hearing loss. This review describes three experiments that point to ROS as a causative factor in both noise- and drug-induced hearing loss and antioxidants as a protective agent. In the first experiment, the ears of chinchillas were treated with R-N6-phenylisopropyladenoisine (R-PIA) and exposed to 150-dB impulse noise. The treated ears developed substantially less permanent hearing loss (PTS) and hair cell loss than the untreated ears. One interpretation of this experiment is that R-PIA increases the availability of glutathione (GSH). In the second experiment, the role of GSH was specifically examined. The ears of chinchillas were treated with glutathione monoethylester (GEE), a pro-GSH drug that has been shown to readily cross cell membranes and increase GSH levels. The GEE-treated ears had significantly less PTS and hair-cell loss than the nontreated ear. Previous research has shown that moderate levels of noise exposure can increase a subject's resistance to noise, and also increase the availability of antioxidant enzymes in the cochlea. In the third experiment, chinchillas were given a series of "toughening" exposures (i.e., 6 h of a 0.5-kHz OB noise at 95 dB for 10 days). After the series of "toughening" exposures, the subjects were treated with carboplatin, a drug that causes massive inner-hair-cell lesions in the chinchilla. The animals receiving the 10-day toughening exposure developed less PTS and hair-cell loss than the control animals.