News Release

Antioxidant-Enhancing Drug Partly Rescues Noise-Induced Hearing Loss

Peer-Reviewed Publication

University at Buffalo

BUFFALO, N.Y. -- Noise-induced hearing loss may be caused partly by free-radical oxidative damage to sensory cells in the inner ear, and a drug called R-PIA can lessen the extent of damage by enhancing antioxidant activity, researchers at the University at Buffalo's Center for Hearing and Deafness have found.

Results of their most recent study, which describes the action of R-PIA in an animal model, will be presented on Friday, Sept. 12, at the Inner Ear Biology Meeting in Bari, Italy.

Donald Henderson, Ph.D., UB professor of communicative disorders and sciences, said the action of R-PIA likely would be similar in the human ear.

"In the future, we may be able to rescue the hearing loss of persons inadvertently exposed to large amounts of noise, such as those near an explosion, for example, through the use of this drug."

Noise-induced hearing loss, a major health problem in industrialized societies, is a primary research focus of UB's Center for Hearing and Deafness, which Henderson co-directs with fellow scientist Richard J. Salvi, Ph.D.

The new study, conducted by Henderson and colleagues Sandra McFadden, Ph.D., and Bo-Hua Hu, Ph.D., along with Richard Kopke, Ph.D., of the U.S. Army, documents the action of R-PIA on noise-induced hearing loss in chinchillas, a mammal with an auditory range similar to that of humans.

In earlier work, the researchers showed that the stress of loud noises causes an increase in free radicals in the inner ear, which can damage or kill sensory cells. To defend themselves, sensory cells express a rush of glutathione, an antioxidant that absorbs free radicals. R-PIA was found to increase the activity of glutathione, thus providing enhanced protection from free-radical damage.

To test the effect of the drug on hearing loss, researchers applied R-PIA topically to the round window (inner-ear membrane) of one group of animals and applied a saline solution as a control in a second group. The animals then were exposed to mid-frequency noise for four hours at levels high enough to cause temporary deafness. The loss of hearing was verified by monitoring brain waves to the hearing center in the cortex. The lack of brain activity in response to normal sound indicated complete hearing loss.

Brain-wave activity was measured again at one day, four days, and 20 days following noise exposure. Results showed that the animals treated with R-PIA recovered their hearing faster and more completely than those treated with saline.

"The R-PIA-treated animals also showed less damage and loss of sensory cells than control animals," Henderson said.

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