Mitochondrial cytochrome oxidase immunolabeling in aged human temporal bones

Citation
Em. Keithley et al., Mitochondrial cytochrome oxidase immunolabeling in aged human temporal bones, HEARING RES, 157(1-2), 2001, pp. 93-99
Citations number
28
Categorie Soggetti
da verificare
Journal title
HEARING RESEARCH
ISSN journal
03785955 → ACNP
Volume
157
Issue
1-2
Year of publication
2001
Pages
93 - 99
Database
ISI
SICI code
0378-5955(200107)157:1-2<93:MCOIIA>2.0.ZU;2-X
Abstract
Presbycusis, an age-related hearing loss, is accompanied by histopathologic al cochlear changes including variable amounts of degeneration of the audit ory receptors, neurons and the stria vascularis. The causes of degeneration are unknown, although acoustic trauma and exposure to ototoxic agents are certainly contributors to the cellular degeneration. Acquired mitochondrial DNA defects are postulated as important determinants of aging in neuromusc ular tissues. The cochlear neurons are highly metabolic and are, therefore, likely to be affected by mitochondrial DNA defects. Sequence analysis has demonstrated a significant number of acquired mutations in the cytochrome o xidase gene in the neurons from aged human cochleas. The current study used immunohistochemical labeling of cytochrome oxidase in the neuronal cell bo dies in archival celloidin sections to evaluate relationships among label d ensity, hearing loss, number of neurons and mitochondrial DNA changes withi n individual cochleas. Label density was less in many aged temporal bones, but not all. There was no relationship among any other variables. It is con cluded that while there may be a decrease in the amount of cytochrome oxida se expression in aged spiral ganglion cell bodies, there are many other fac tors that contribute to hearing loss and cellular degeneration. (C) 2001 El sevier Science B.V. All rights reserved.