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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