mitochondrial theory of aging

Doug Skrecky oberon at
Wed Mar 8 21:25:48 EST 2000

Citations: 1-2
  Gershon D.
  Department of Biology, Technion-Israel Institute of Technology, Haifa,
  The mitochondrial theory of
  aging: is the culprit a faulty disposal system rather than
  indigenous mitochondrial alterations? [comment]. [Review]
  [16 refs]
  Comment on: Exp Gerontol 1999 Aug;34(5):605-12
  Experimental Gerontology.  34(5):613-9, 1999 Aug.
  Mitochondrial damage and the proportion of effete
  mitochondria in cells increase with age. According to the
  mitochondrial theory of
  aging, this phenomenon is mostly due to oxidative damage and
  is a major (and, some argue, the main) determinant of aging.
  It will be argued briefly that this phenomenon plays a role that is not
  exclusively crucial in aging. It will also be contended,
  essentially on theoretical grounds (for lack of sufficient current
  information), that there is low probability that the accumulation of reduced
  degradation of affected mitochondria is due to diminished production of
  hydroxyl radicals, as suggested by Aubrey and de Grey (1997) and expanded by
  Kowald (in this issue). What seems more likely is that the phagolysosomal
  disposal system of effete mitochondria is considerably altered in cells of
  aging organisms. Also, in view of the significant role of
  damaged mitochondria in the initial steps in apoptosis and the lack of
  evidence of massive apoptosis of cells in senescent individuals, the damage
  that exists may be milder than anticipated by the
  mitochondrial theory of
  aging. A brief fundamental summary on the biology of
  mitochondria is included for the sake of better understanding the arguments
  presented in this article. Also, suggestions are made for experimental
  testing of the hypotheses presented by Aubrey and de Grey (1997) and Kowald
  (1999). [References: 16]

  Kowald A.
  Innovationskolleg Theoretische Biologie, Humboldt University Berlin, Germany.
  The mitochondrial theory of
  aging: do damaged mitochondria accumulate by delayed
  degradation? [see comments]. [Review] [42 refs]
  Comment in: Exp Gerontol 1999 Aug;34(5):613-9
  Experimental Gerontology.  34(5):605-12, 1999 Aug.
  The mitochondrial theory of
  aging states that the slow accumulation of impaired
  mitochondria is the driving force of the aging process. In
  recent years, this theory has gained new support with the
  discovery of age-related mitochondrial DNA deletions.
  However, the underlying mechanism of the accumulation of defective
  mitochondria remained unclear. This has changed recently with the proposal of
  de Grey that damaged mitochondria have a decreased degradation rate. The
  resulting increase in biological half-life would be a strong selection
  advantage leading to the accumulation of defective mitochondria. In this
  article, I summarize current ideas on how damaged organelles can build up in
  a cell as well as the shortcomings of these ideas. Then the new hypothesis
  and its justification are described. It appears that de Grey's hypothesis is
  a very promising concept that elegantly solves inconsistencies of current
  models and is in accordance with experimental findings. [References: 42]

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