کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
9881235 1535692 2005 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Lack of age-related increase of mitochondrial DNA amount in brain, skeletal muscle and human heart
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
پیش نمایش صفحه اول مقاله
Lack of age-related increase of mitochondrial DNA amount in brain, skeletal muscle and human heart
چکیده انگلیسی
During the ageing process, an increase of mitochondrial DNA (mtDNA) deletions and other mutations have been reported. These structural alterations of mtDNA are assumed to cause a reduction in the respiratory chain activity and may contribute to the ageing process. Therefore, the question arises if the accumulation of deleted mtDNA is compensated in vivo by an increase of mtDNA synthesis via a feedback mechanism. We designed two human mtDNA-specific oligonucleotide probes for quantitative mtDNA analysis of 5 different tissues from 50 individuals aged from 8 weeks to 93 years. The amount of mtDNA was approximately 1.1 ± 0.5% (4617 ± 2099 copies) in the caudate nucleus, 1.0 ± 0.5% (4198 ± 2099 copies) in the frontal lobe cortex, 0.3 ± 0.2% (1259 ± 840 copies) in the cerebellar cortex, 1.0 ± 0.4% (4198 ± 1679 copies) in skeletal muscle and 2.2 ± 1.3% (9235 ± 5457 copies) in heart muscle. We did not observe any significant change in the absolute copy number during ageing in five different tissues, and therefore, found no evidence for the postulated feedback mechanism. Our study indicates that mtDNA copy number is tissue-specific and depends on the energy demand of the tissue.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mechanisms of Ageing and Development - Volume 126, Issue 11, November 2005, Pages 1192-1200
نویسندگان
, , , , , ,