Mitochondrial cytochrome oxidase immunolabeling in aged human temporal bones

Keithley, Elizabeth M.; Harris, Brandy; Desai, Keyur; Linthicum, Fred H.; Fischel‐Ghodsian, Nathan

doi:10.1016/s0378-5955(01)00281-7

Cited by 15 publications

(12 citation statements)

References 24 publications

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“…Approximately 50% of cases of AHL represent a pure sensory, neural, or strial presbycusis, 25% a mixture of two or more types, and in the remaining 25% of cases the pathology does not correlate with the audiogram. This histological variety observed in AHL cases and degree of variability in both quantity and quality of cellular degeneration within genetically and environmentally homogeneous populations of animals provide indirect evidence of genetic heterogeneity (Fischel-Ghodsian et al, 1997;Keithley et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss

et al. 2007

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Section: Introductionmentioning

confidence: 99%

Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss

et al. 2007

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“…The expression of the partially mitochondrially encoded enzyme cytochrome oxidase was found not to be reduced in archival temporal bones from presbyacusis patients, as assessed by antibody staining [Keithley et al, 2001]. This contrasts with the position in muscle, where the degree of cytochrome oxidase functional activity, as determined histochemically, decreases with ageing.…”

Section: Changes In Aged Human Inner Earsmentioning

confidence: 59%

Mutation in Mitochondrial DNA as a Cause of Presbyacusis

Pickles¹

2003

Audiol Neurotol

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Much of the hearing loss that occurs in old age is likely to be due to the long-term deterioration of the mitochondria in the different structures of the cochlea. The current review surveys some of the basic information on mitochondria and mitochondrial DNA, as a background to their possible involvement in presbyacusis. It is likely that oxygen radicals damage mitochondrial DNA and other components of the mitochondria, such as their proteins and lipids. This further compromises both oxidative phosphorylation and the repair processes in mitochondria, setting up a vicious cycle of degradation. Evidence is presented from inherited point mutations on the possibly most critical sites for mutations in mitochondrial DNA associated with hearing loss. It is suggested that random sorting and clonal expansion of mutations both maintain the integrity of the pool of mitochondrial DNA molecules and give rise to the apoptosis that leads to loss of vulnerable cells, and hence to deafness. It is moreover suggested that apoptosis of the vulnerable cells of the inner ear may to some extent be preventable, or at least delayed.

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“…Changes in cytochrome C IR with age have been detected in the human temporal bone (Keithley et al, 2001). The ubiquitous presence of Tom20 in the inner ear and decreased Tom20-IR in temporal bones from older patients with Meniere's disease, support the idea that a mitochondrial dysfunction may be a contributor of hearing loss in Meniere's disease.…”

Section: Tom20 Immunolocalization In the Inner Earmentioning

confidence: 82%

Immunocytochemical Localization of the Translocase of the Outer Mitochondrial Membrane (Tom20) in the Human Cochlea

Balaker

Ishiyama

López

et al. 2012

The Anatomical Record

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Mitochondrial degeneration in the inner ear is likely a contributing factor in age-related hearing loss and other otopathologies such as Meniere's disease. Most mitochondrial proteins are synthesized in the cytosol and imported through the mitochondrial membranes by translocators. The translocase of the outer membrane (Tom) is the universal entry gate for all proteins that are imported into mitochondria. Altered function of the translocator could alter protein transport into the mitochondria, and disrupt function. In this study, we determined the immunolocalization of Tom20, a major mitochondrial protein import receptor, in microdissected human cochlea frozen sections obtained from postmortem autopsy and celloidin-embedded archival specimens. We used affinity purified rabbit polyclonal antibodies against Tom20. We also determined the Tom20 immunolocalization in the mouse inner ear. In the human and mouse cochlea, Tom20 was ubiquitously distributed in the organ of Corti, allowing well-delineated visualization of inner and outer hair cells. Tom20 immunoreactivity localized in the cytoplasm of spiral ganglia neurons. In the inner ear of aged subjects with Meniere's disease, there was decreased expression of Tom20. These results suggest that Tom20 can be used in the inner ear as a marker for mitochondrial protein import. Anat Rec,

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Mitochondrial cytochrome oxidase immunolabeling in aged human temporal bones

Cited by 15 publications

References 24 publications

Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss

Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss

Mutation in Mitochondrial DNA as a Cause of Presbyacusis

Immunocytochemical Localization of the Translocase of the Outer Mitochondrial Membrane (Tom20) in the Human Cochlea

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