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A proposed mechanism of the gene Ahl for increased susceptibility to noise-induced hearing loss.

Authors
Davis-RR; Kozel-P; Erway-LC
Source
Abstr 26th Midwinter Res Meet 2003 Feb; 22:131-132
NIOSHTIC No.
20041685
Abstract
Animals and humans show differing susceptibility to noise damage even under very carefully controlled exposure conditions. This difference in susceptibility may be related to an uncontrolled genetic component. Common experimental animals (rats, guinea pigs, chinchillas, cats) are outbred?their genomes contain an admixture of many genes. About 10 years ago Erway et al (1993) demonstrated a recessive gene associated with early presbycusis in inbred mice: Ahl. A series of studies have shown that mice homozygous for Ahl are more sensitive to the damaging effects of noise. Recent work has shown that mice homozygous for Ahl are not only more sensitive to noise, but also are probably damaged in a different manner by noise than mice containing the wild-type gene. Recent work in Noben-Trauth?s lab (Di Palma et al., 2001) has shown that the wild-type Ahl gene codes for an outer-hair cell specific cadherin. Cadherins are calcium dependent proteins which hold cells together at adherins junctions to form tissues and organs. The cadherin of interest is localized to outer hair and has been termed otocadherin or cdh-23. Reduction in, or missing otocadherin may allow stereocilia to be more easily physically damaged by loud sounds and by aging.
Keywords
Noise-exposure; Exposure-levels; Noise-induced-hearing-loss; Noise-exposure; Noise; Hearing; Hearing-disorders; Hearing-loss; Laboratory-animals; Animals; Cell-damage; Cellular-reactions; Animal-studies
Publication Date
20030222
Document Type
Abstract
Editors
Santi-PA
Funding Type
Grant
Fiscal Year
2003
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-R01-OH-003973
ISSN
0742-3152
Source Name
Abstracts of the 26th Midwinter Research Meeting
State
FL; NJ; MO; OH
Performing Organization
Washington University
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