mitochondrial theory of aging

rjk3 rjk3 at my-deja.com
Thu Mar 9 09:46:27 EST 2000


I wonder what Aubrey and de Grey (sic) have to say about this.

  Richard

In article <8a723c$8ge$1 at sylvester.vcn.bc.ca>,
  Doug Skrecky <oberon at vcn.bc.ca> wrote:
> Citations: 1-2
> <1>
> Authors
>   Gershon D.
> Institution
>   Department of Biology, Technion-Israel Institute of Technology,
Haifa,
>   Israel.
> Title
>   The mitochondrial theory of
>   aging: is the culprit a faulty disposal system rather than
>   indigenous mitochondrial alterations? [comment]. [Review]
>   [16 refs]
> Comments
>   Comment on: Exp Gerontol 1999 Aug;34(5):605-12
> Source
>   Experimental Gerontology.  34(5):613-9, 1999 Aug.
> Abstract
>   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]
>
> <2>
> Authors
>   Kowald A.
> Institution
>   Innovationskolleg Theoretische Biologie, Humboldt University Berlin,
Germany.
> Title
>   The mitochondrial theory of
>   aging: do damaged mitochondria accumulate by delayed
>   degradation? [see comments]. [Review] [42 refs]
> Comments
>   Comment in: Exp Gerontol 1999 Aug;34(5):613-9
> Source
>   Experimental Gerontology.  34(5):605-12, 1999 Aug.
> Abstract
>   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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