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English Abstract
Journal Article
Research Support, Non-U.S. Gov't
[Mitochondrial DNA4977 deletions associated with human presbycusis].
Zhonghua Er Bi Yan Hou Ke za Zhi 2000 December
OBJECTIVE: To determine whether or not the mtDNA4977 deletions contribute to human aging and involve in the development of presbycusis.
METHODS: 67 sides of archival temporal bone sections, 20 temporal brains, 21 cochlear nucleus, 20 hearts and 22 livers were harvested and the total DNA was extracted. The presence of mtDNA4977 deletions was examined using nest polymerase chain reaction(PCR).
RESULTS: Our results showed: (1) the highly conserved mitochondrially-encoded tRNA and ND1 segments were amplified from all tissues, as well as mtDNA4977 deletions related to aging. (2) The incidence of carrying mtDNA4977 deletions in all tissues in aged group was significant higher than that of young control group (P < 0.05). (3) The incidence of carrying mtDNA4977 deletions in temporal bone sections and cochlear nucleus with presbycusis patients was significant higher than that of aged normal hearing control group (P < 0.05). However, the incidence of carrying mtDNA4977 deletions in heart and liver were no significant difference between presbycusis patients and the control group.
CONCLUSION: These findings indicated that mtDNA4977 deletions in human contribute to presbycusis, as well as aging.
METHODS: 67 sides of archival temporal bone sections, 20 temporal brains, 21 cochlear nucleus, 20 hearts and 22 livers were harvested and the total DNA was extracted. The presence of mtDNA4977 deletions was examined using nest polymerase chain reaction(PCR).
RESULTS: Our results showed: (1) the highly conserved mitochondrially-encoded tRNA and ND1 segments were amplified from all tissues, as well as mtDNA4977 deletions related to aging. (2) The incidence of carrying mtDNA4977 deletions in all tissues in aged group was significant higher than that of young control group (P < 0.05). (3) The incidence of carrying mtDNA4977 deletions in temporal bone sections and cochlear nucleus with presbycusis patients was significant higher than that of aged normal hearing control group (P < 0.05). However, the incidence of carrying mtDNA4977 deletions in heart and liver were no significant difference between presbycusis patients and the control group.
CONCLUSION: These findings indicated that mtDNA4977 deletions in human contribute to presbycusis, as well as aging.
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