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is cell aging caused by respiration-dependent injury to the mitochondrial genomeThough intrinsic mitochondrial aging has been considered before as a possible cause of cellular senescence, the mechanisms of such mitochondrial aging have remained obscure. In this article, the hypothesis of free-radical-induced inhibition of mitochondrial replenishment in fixed postmitotic cells is expanded. It is maintained that the respiration-dependent production of superoxide and hydroxyl radicals may not be fully counteracted, leading to a continuous production of lipoperoxides and malonaldehyde in actively respiring mitochondria. These compounds, in turn, can easily react with the mitochondrial DNA which is in close spatial relationship with the inner mitochondrial membrane, producing an injury that the mitochondria may be unable to counteract because of their apparent lack of adequate repair mechanisms. Mitochondrial division may thus be inhibited leading to age-related reduction of mitochondrial numbers, a deficit in energy production with a concomitant decrease in protein synthesis, deterioration of physiological performance, and, therefore, of organismic performance.
Document ID
Document Type
Reprint (Version printed in journal)
Fleming, J. E.
(San Jose State Univ. CA, United States)
Yengoyan, L. S.
(San Jose State University San Jose, CA, United States)
Miquel, J.
(NASA Ames Research Center Moffett Field, CA, United States)
Cottrell, S. F.
(Brooklyn College Brooklyn, NY, United States)
Economos, A. C.
(Louvain, Universite Catholique, Louvain-la-Neuve, Belgium)
Date Acquired
August 11, 2013
Publication Date
January 1, 1982
Publication Information
Publication: Gerontology
Volume: 28
Subject Category
Distribution Limits