[tt] [x-risk] Life-extending protein can also have damaging effects on brain cells
Eugen Leitl
<eugen at leitl.org> on
Wed Jul 2 06:41:02 UTC 2008
----- Forwarded message from arsen zahray <menkaur at gmail.com> -----
From: arsen zahray <menkaur at gmail.com>
Date: Wed, 2 Jul 2008 05:07:45 +0300
To: existential at transhumanism.org
Subject: [x-risk] Life-extending protein can also have damaging effects on
brain cells
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Reply-To: For discussion of existential risks <existential at transhumanism.org>
[1]http://www.physorg.com/news134135331.html
Proteins widely believed to protect against aging can actually cause
oxidative damage in mammalian brain cells, according to a new report
in the July Cell Metabolism, a publication of Cell Press. The findings
suggest that the proteins can have both proaging and protective
functions, depending on the circumstances, the researchers said.
" Sirtuins are very important proteins," said Valter Longo of the
University of Southern California, Los Angeles. "Overexpression can
protect in some cases, and in other cases, it may do the opposite. It
has to do with the fact that they do so many things."
Sirtuins, or Sir2 family proteins, are found in organisms from
bacteria to humans. Sir2 controls aging and life span in yeast, the
worm C. elegans, and Drosophila fruit flies, earlier studies have
shown.
Studies have also implicated Sir2 in the life-extending effects of a
calorie restricted diet in some, though not all, organisms. Notably,
Longo's lab showed that lack of Sir2 in yeast further extended the
life span of calorie-restricted cells.
SirT1, the mammalian version of yeast Sir2, controls numerous
physiological processes including glucose metabolism, DNA repair, and
cell death, the researchers added. In mammalian cells, SirT1 also
controls several stress-response factors.
Now, the researchers show that cultured rat neurons treated with a
SirT1 inhibitor more often survived treatment with oxidative
stress-inducing chemicals. They further show evidence to explain the
mechanism responsible for that effect.
They also found lower oxidative stress levels in the brains of mice
without SirT1. However, those SirT1 knockout mice didn't live as long
as normal mice do on either a normal or a calorie-restricted diet.
" [Such drugs] could have beneficial effects for certain diseases, but
again, these proteins do a lot of things," he said. "I would say the
idea that there is a conserved action of sirtuins to cause major life
span extension--the foundations for that are weak or very weak. Until
we have more data to show that chronic treatment to increase SirT1
activity does not do damage, I don't think it's a good idea."
References
1. http://www.physorg.com/news134135331.html
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