Tissue-specific Distribution of Multiple Mitochondrial DNA Rearrangements during Human Aging

Mitochondria, according to the free radical theory of aging, are the major source of reactive oxygen species (ROS). The results, presented in this paper, question the role of reactive oxygen species in contributing significantly to the extent of mitochondrial bioenergy degradation of the tissues, wh...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 1998-11, Vol.854 (1), p.171-181
Main Authors: KOVALENKO, SERGEY A., KOPSIDAS, GEORGE, KELSO, JOANNE, ROSENFELDT, FRANKLIN, LINNANE, ANTHONY W.
Format: Article
Language:English
Subjects:
Aged
Aging - genetics
Animals
DNA Damage
DNA, Mitochondrial - genetics
Electron Transport Complex IV - genetics
Electron Transport Complex IV - metabolism
Humans
Mitochondria - genetics
Mitochondria - metabolism
Mitochondria, Heart - genetics
Mitochondria, Heart - metabolism
Mitochondria, Liver - genetics
Mitochondria, Liver - metabolism
Mitochondria, Muscle - genetics
Mitochondria, Muscle - metabolism
Mutation
Organ Specificity
Reactive Oxygen Species - metabolism
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Summary:Mitochondria, according to the free radical theory of aging, are the major source of reactive oxygen species (ROS). The results, presented in this paper, question the role of reactive oxygen species in contributing significantly to the extent of mitochondrial bioenergy degradation of the tissues, which can be correlated with mtDNA rearrangements. We report here that mtDNA rearrangements, including deletions and duplications, in tissues from human aged subjects, occur in levels ranging from very low in liver, to considerable in cardiac muscle, to almost total in skeletal muscle. The extent of mtDNA rearrangements is correlated at both the individual tissue and cell level with cytochrome oxidase (COX) activity as the exemplifier of cellular bioenergy capacity. Thus, the ROS proposal in its simplest form as it affects mtDNA and mitochondrial electron transport system is not supported by the available data.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.1998.tb09900.x