ST. PETERSBURG, FLA. -- Age-related hearing loss may be lessened or prevented in the future by regulating an enzyme that neutralizes free-oxygen radicals, destructive molecules that can destroy sensory hair cells of the inner ear, suggests preliminary research conducted in the University at Buffalo's Center for Hearing and Deafness.

Using mice lacking one or both components of the genes responsible for production of the antioxidant enzyme superoxide dismutase, or SOD, the UB researchers showed that age-related hearing loss was greater and progressed faster in mice deficient in the enzyme than in mice with a normal genetic makeup and SOD production that served as a control group.

Results of the research were presented here today (Tuesday, Feb. 17) at the annual meeting of the Association for Research in Otolaryngology.

"Before this present study, we thought that hearing loss was a normal process of aging," said Richard Salvi, Ph.D., co-director of the Center for Hearing and Deafness and leader of the research group.

"Then we found people with no loss, and we figured it was related to a low-noise environment. Now we believe that at least some age-related hearing loss is due to a genetic deficiency in antioxidant enzymes, such as SOD. If we are able to regulate the enzyme and modulate the number of free radicals present, there is hope for a therapy for age-related hearing loss. "

To arrive at their findings, the researchers used mice in which one or both components of the gene responsible for production of SOD had been eliminated, along with mice with a normal amount of SOD.

"Mice are good models for studying human hearing loss," said Sandra McFadden, Ph.D., a researcher in the study group, "because like humans, they lose hearing at high frequencies first, while hearing loss in most other animals begins in the lower frequencies."

In one study, the researchers measured auditory
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Contact: Lois Baker
baker@newsb.buffalo.edu
716-645-2626
University at Buffalo
17-Feb-1998