From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Wed Mar 08 2000 - 02:06:15 MST
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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