I have to diagree with Steve's interpretation here. There is nothing wrong
with calling something the "free radical theory of aging" just because SOME
of our cells CAN deal with the free radicals. True, that does mean that in
SOME cells the problem could be interpreted as lack of a system/ability
which other cells have. So? In the cells in question the "Free Radical
Theory of Aging" is still a perfectly accurate name (and I would submit
that "in the cells in question" is all that we can worry about, or assign a
name to, because the causes of aging likely vary from cell type to cell
type).
If I am understanding you correctly, you would prefer that it be called
something like the "I'm not dividing and that is causing problems Theory of
Aging."
And that might be OK too. But I tend to look at these things from a "How
can we solve the problem?" point of view. So instantly two options come to
mind as a result of this discussion. First, we can fix these cells by
making them divide. Second, we can try to reduce/eliminate free radical
damage.
Certainly the second possibility is more likely to be physiologically
relevant, since you can't very well tell all your post-mitotic cell types
to start dividing again (and expect to live). Free radicals are the
RELEVANT concern, even though you could make an argument that they are not
necessarily the universal root of the problem. So the name of the theory
is more accurate as it stands.
James
[snip]
>>>> >Convincing though this may sound on the surface, it is completely
> >wrong. The cells in the human body which appear to suffer
> >mitochondrial damage are the non-dividing (or rarely-dividing) ones;
> >the rapidly dividing ones remain mitochondrially healthy. Our
> >possession of (and reliance on) cell types which do not divide is,
> >according to the mitochondrial theory
> >of aging, the thing that renders us vulnerable.
>> Comment:
>> Then all I can say is that it's a really stupidly named "theory."
> If failure of cells to divide led to non-repair of membranes (which
> otherwise happens in dividing cells), would you call this the
> "membrane" theory of aging? If failure of cells to divide led to non
> repair of of DNA, would you call this the "DNA theory of aging?" If
> non division let to protein turnover problems and clinker enzymes,
> would you refer to this as the error catastrophe theory of aging?
>> Though all these mistakes have been made in gerontology, I hope you
> would not perpetuate them, since in all cases it's clear that the
> damage problem is secondary to the failure of repair, which in dividing
> cells does not even exist. Repair in many dividing cells is quite
> sufficient for functional immortality, and I can hardly overemphasize
> this point. Thus, if failure of this repair process to keep up with
> free radical damage in non-dividing cells leads to increasing free
> radical damage, it's simply obfuscatory to refer to this as a "free
> radical" theory of aging. Free radicals are not the primary problem in
> that case. If your gardner doesn't spray for bugs and the bugs eat
> your garden, you don't say you have a bug problem. If you're
> intelligent you realize that you have a gardener problem. Go to
> primary sources. Since some cells deal with free radicals well enough
> to be immortal, free radicals are not the primary cause of aging. They
> are intermediate cause of damage when the PRIMARY problem (whatever it
> is) interfers with the repair systems which keep radical damage from
> accumulating.
>> Hope my position is now clear.
>> Steve Harris, M.D.
>
