From: Ramez Naam (mez@apexnano.com)
Date: Tue Apr 29 2003 - 22:59:10 MDT
From: Robert J. Bradbury [mailto:bradbury@aeiveos.com]
> For many years I have always suspected there was a reason
> that antioxidant vitamin supplements (Vit E, C, etc.) didn't
> extend lifespan more. I ran across hints that various
> oxidized molecules such as superoxide or hydrogen peroxide
> might be used as signal molecules and the genetic program was
> designed to keep them within certain ranges.
>
> Well, now I finally have a concrete example of this. Others
> on the list may have been more aware of this but I was not so
> I'm sharing it.
[snip much good content]
> The bottom line from my perspective is that if the cell
> wants to use H2O2 as a signaling molecule it will do so and
> taking all the Vitamin E and C in the world isn't going to
> prevent that. (Which isn't to say that Vitamin E might be
> highly useful to keep cholesterol from becoming oxidized
> and contributing to the formation of plaques). It seems
> unlikely that antioxidants are going to impact much on
> oxidative damage to DNA (and therefore cancer and some
> aspects of aging).
Fascinating! Thanks for posting, Robert. I hadn't caught these
papers.
It's strange, though, that up-regulation of endogenous anti-oxidants
/does/ slow aging. We know of a couple fruit fly models and at least
one mouse model where the organisms have been genetically engineered
to have higher levels of superoxide dismutase or catalase, and have
(apparently as a result) had slower aging, longer mean and maximum
lifespan, and greater resistance to stress.
In the mouse model, the catalase is specifically targeted to the
mitochondria. The fact that upregulating endogenous anti-oxidants in
the mitochondria extends life seems to support the mitochondrial free
radical theory of aging.
So do you have any thoughts on why that those mutant creatures are
life extended, as it pertains to your post above?
cheers,
mez
This archive was generated by hypermail 2.1.5 : Tue Apr 29 2003 - 23:11:03 MDT