期刊
MECHANISMS OF AGEING AND DEVELOPMENT
卷 130, 期 5, 页码 343-349出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2009.01.008
关键词
Mitochondrial genome mutation; Hypothesis of aging; Real-time quantitative PCR; Mitochondrial genome deletions; Mitochondrial replication; Mitochondrial transcription
资金
- Hunter Medical Research Institute
- University of Newcastle
- Research Grants Scheme
- Clive and Vera Ramaciotti Foundation
Impaired mitochondrial oxidative phosphorylation (OXPHOS) is considered a cause of aging. A reduction in mitochondrial DNA (mtDNA) replication and/or transcription may contribute to this OXPHOS diminution. Impairments in the displacement (D) loop, or non-coding, region of the mitochondrial genome, or accumulation of mtDNA mutations, may affect mtDNA replication and transcription. We determined the effects of age on the D-loop and on mtDNA deletion mutations in the spinal cord, medulla, midbrain, cerebellum, striatum, and cerebral cortex of Fischer 344 rats. D-loop, 7S DNA levels were reduced by 3-fold in striatum, 2.5-fold in cortex, and 2-fold in the spinal cord of older animals. We did not detect a population of mtDNA affected by the most prevalent known (ND4-containing) deletions, indicating they do not comprise a significant portion of total mtDNA. However, we detected an age-related and region-specific increase in the common deletion, which comprised 0.0003-0.0007% of total mtDNA. Mitochondrial genome copy number varied between regions, in addition to an overall 18% decrease with age across the whole brain. These results suggest the age-related decline in OXPHOS may be related to a reduction in D-loop function. Crown Copyright (C) 2009 Published by Elsevier Ireland Ltd. All rights reserved.
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