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[Cochlear hypoxia and mtDNA deletion: possible correlated factors to cause presbycusis].
Zhonghua Yi Xue za Zhi [Chinese medical journal] 2000 December
OBJECTIVE: To find the relationship among the most common mitochondrial DNA (mtDNA) 4,977 bp deletion, aging and deterioration of acoustic organ and determine the pathologic factors causing mtDNA 4,977 bp deletion.
METHODS: Sixty-seven temporal bones from a presbycusis group, an age-matched control group and a young control group were evaluated. The nested PCR and tri-nested PCR techniques were used to test the presence of mtDNA 4,977 deletion. Computer imaging processing was used to measure the parameters of blood vessels in the internal acoustic meatus.
RESULTS: Temporal bones from patients aged 50 years or over frequently showed mtDNA 4,977 deletions. In presbycusis patients, 17 of 34 ears showed mtDNA 4,977 deletion, whereas only 4 of 19 ears from the age-matched control group showed mtDNA 4,977 deletions. mtDNA 4,977 deletions were often seen in the spiral ganglion and vestibular ganglion neurons. In the presbycusis group, the lumen of the vasa nervosum of the internal auditory meatus showed a more severe reduction in patients with mtDNA 4,977 deletion than in those without deletion.
CONCLUSION: There is a strong correlation between presbycusis and mtDNA 4,977 deletion. We hypothesize that cochlear hypoxia may cause mtDNA 4,977 deletions and other mtDNA mutants which in turn may cause a reduction of mitochondrial oxidative phosphorylation and decreased auditory nerve function. The symptoms of neural presbycusis, however, may appear only after mtDNA metabolism decreases below a specific threshold.
METHODS: Sixty-seven temporal bones from a presbycusis group, an age-matched control group and a young control group were evaluated. The nested PCR and tri-nested PCR techniques were used to test the presence of mtDNA 4,977 deletion. Computer imaging processing was used to measure the parameters of blood vessels in the internal acoustic meatus.
RESULTS: Temporal bones from patients aged 50 years or over frequently showed mtDNA 4,977 deletions. In presbycusis patients, 17 of 34 ears showed mtDNA 4,977 deletion, whereas only 4 of 19 ears from the age-matched control group showed mtDNA 4,977 deletions. mtDNA 4,977 deletions were often seen in the spiral ganglion and vestibular ganglion neurons. In the presbycusis group, the lumen of the vasa nervosum of the internal auditory meatus showed a more severe reduction in patients with mtDNA 4,977 deletion than in those without deletion.
CONCLUSION: There is a strong correlation between presbycusis and mtDNA 4,977 deletion. We hypothesize that cochlear hypoxia may cause mtDNA 4,977 deletions and other mtDNA mutants which in turn may cause a reduction of mitochondrial oxidative phosphorylation and decreased auditory nerve function. The symptoms of neural presbycusis, however, may appear only after mtDNA metabolism decreases below a specific threshold.
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