Abstract |
In mammalian cells, there is an extensive and continuous exchange of mitochondrial DNA ( mtDNA) and its products between mitochondria. This mitochondrial complementation prevents individuals from expression of respiration deficiency caused by mutant mtDNAs. Thus, the presence of mitochondrial complementation does not support the generally accepted mitochondrial theory of aging, which proposes that accumulation of somatic mutations in mtDNA is responsible for age-associated mitochondrial dysfunction. Moreover, the presence of mitochondrial complementation enables gene therapy for mitochondrial diseases using nuclear transplantation of zygotes.
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Authors | Akitsugu Sato, Kazuto Nakada, Jun-Ichi Hayashi |
Journal | Biochimica et biophysica acta
(Biochim Biophys Acta)
2006 May-Jun
Vol. 1763
Issue 5-6
Pg. 473-81
ISSN: 0006-3002 [Print] Netherlands |
PMID | 16624428
(Publication Type: Journal Article, Review)
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Chemical References |
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Topics |
- Aging
(genetics, metabolism, pathology)
- Animals
- DNA, Mitochondrial
(genetics)
- Genetic Therapy
- Humans
- Mitochondria
(genetics, metabolism, pathology)
- Mitochondrial Diseases
(genetics, pathology, therapy)
- Mutation
(genetics)
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