| Literature DB >> 16624428 |
Akitsugu Sato1, Kazuto Nakada, Jun-Ichi Hayashi.
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.Entities:
Mesh:
Substances:
Year: 2006 PMID: 16624428 DOI: 10.1016/j.bbamcr.2006.03.001
Source DB: PubMed Journal: Biochim Biophys Acta ISSN: 0006-3002