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 sensory-cell loss in mice that were young (2 months), middle-aged (7 months) and aged (17 months). None were subjected to any interventions, such as noise exposure, that could cause cell damage, yet researchers found dramatic differences among the groups
"The control-group mice had some sensory-cell loss just from being old, but far less than the mice lacking SOD," said Robert Burkhard, Ph.D., a principal researcher on the study. "This suggests that SOD may play a role in cell loss, a condition that leads to hearing loss. People who have deficiencies in SOD or other antioxidant enzymes may be at greater risk for losing their hearing."
In a companion study, researchers lead by McFadden measured actual hearing loss, as well as sensory-cell loss, in mice that were 13-months-old, an age roughly equivalent to 50-60 human years. As in the previous study, none of the mice had been exposed to interventions that could affect hearing.
Mice lacking one component of the SOD gene had greater hearing loss than the control-group mice, particularly at the higher frequencies, results showed. The mice lacking both genes were very likely to be deaf at 13 months.
"We know that the free radicals produced throughout the body as by-products of normal cell metabolism can cause extensive damage to living tissues, including the sensory hair cells in the inner ear, if they are not neutralized by antioxidant enzymes," McFadden said. "We think that SOD deficiencies may increase cochlear vulnerability to environmental insults, such as noise or drugs, as well as to injury from normal free-radical activity during aging.
"An increase in antioxidant enzymes that neutralize free radicals, such as SOD, may protect the cochlea from these insults and prevent or lessen hearing loss."
McFadden has received a grant from the National Organization for Hearing Research to study the relationship between noise and aging in the production of hearing loss in SOD-deficient mice.
Other contributors to the study were Dalian Ding, UB research support specialist, and Cephalon Inc., of West Chester Pa., developer of the SOD-deficient mice.
The studies were funded by the National Institutes of Health.
The above post is reprinted from materials provided by University At Buffalo. Note: Materials may be edited for content and length.
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