Current Research Into Telomeres III
Aubrey de Grey
ag24 at mole.bio.cam.ac.uk
Fri Sep 4 08:41:51 EST 1998
> From what I understand mice and other animals put on caloric
> restriction lived longer because they had less free radical damage.
I wouldn't yet go quite so far as "because", but certainly there is a
consensus that this is a large part of the reason.
> Now, what would be interesting to find out is "why" having less free
> radical damage lengthens lifespan.
I don't really agree. I think what would be much more interesting
is to find out why (or how) caloric restriction reduces free radical
damage. We haven't been very successful in reducing free radical
damage by antioxidant therapy, for example; caloric restriction may
be doing something we haven't thought of but which we could emulate.
> Has there been any work done to see if
> in elderly individuals there is an accumilation of free radical damage
> in their cells?
Certainly, masses. And yes, there is -- especially in the non-dividing
cells and the ones that use a lot of oxygen.
> Free Radical Damage and AGE
> accumulation increases with age because the cells in the human body
> telomeres shorten, grow older, and produce more free radicals, cannot
> protect themselves from free radicals as well, and cannot get rid of
> AGE's as well.
A fine theory except for the size of its gaps. We don't yet have any
plausible, *detailed* hypothesis for a mechanism whereby short-telomered
cells would produce more free radicals in such a way as to harm cells
that aren't dividing. We're not exactly spoilt for detailed hypotheses
whereby a small number of mitochondrially defunct cells would do this,
either, but at least there's one (in my JAAM article). The importance
of detail, of course, is that it gives both easier testability and more
opportunity to design interventions.
Aubrey de Grey
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