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Biological Chemistry

Preventing Cell Death Halts Hearing Loss

Antioxidants suppress a protein that initiates apoptosis in inner ear neurons, stopping hearing loss in mice

by Sophie L. Rovner
November 16, 2009 | A version of this story appeared in Volume 87, Issue 46

More than 40% of Americans older than 65 suffer from age-related hearing loss, which is associated with the death of irreplaceable spiral ganglion neurons and other cells in the inner ear. A team of researchers has now elucidated the molecular mechanism underlying the condition (Proc. Natl. Acad. Sci. USA, DOI: 10.1073/pnas.0908786106). One theory of aging posits that reactive oxygen species inflict cumulative mitochondrial damage that contributes to aging. Furthermore, accumulation of mitochondrial DNA mutations has been shown to be a factor in age-related hearing loss. In the new study, geneticist Tomas A. Prolla of the University of Wisconsin, Madison, and colleagues found that reactive oxygen species trigger expression of the protein Bak in ear cells in mice. This protein initiates apoptosis, or programmed cell death, in the cells. Feeding the mice antioxidants such as α-lipoic acid or coenzyme Q10—which suppress expression of Bak—prevented apoptosis and hearing loss. The results suggest that these compounds could be used to avert hearing loss in people.


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