From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Wed Apr 30 2003 - 05:22:50 MDT
On Tue, 29 Apr 2003, Ramez Naam wrote:
> 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?
I think you may have answered your own question -- anti-oxidants or
anti-oxidant defenses may work best if targeted. Most likely the
best targets are locations where the small oxidizing molecules are
not used as signal molecules. One of the papers mentioned that H2O2
seems to be involved in the NfKB signal pathway which I'm fairly sure
is cytosolic, and perhaps nuclear. So beefing up mitochondrial defenses
may have little downside. I think researchers also ran into this when
beefing up SOD activity in that they found things worked better if
they only did it in specific tissues (perhaps those that do not
typically use small oxidizing molecules as signal molecules).
Of course with typical dietary antioxidants they are not targeted
so the results may be much less specific/effective.
Robert
This archive was generated by hypermail 2.1.5 : Wed Apr 30 2003 - 05:33:58 MDT