cron-web.org

[A1CR]

It appears that the http://en.wikipedia.org/wiki/Glutathione
http://en.wikipedia.org/wiki/Redox status alters such that
areas of the
brain subject to various brain diseases that increase with
aging are
countered by CR.

Rebrin I, Forster MJ, Sohal RS.
Effects of age and caloric intake on glutathione redox state
in different
brain regions of C57BL/6 and DBA/2 mice.
Brain Res. 2006 Nov 16; [Epub ahead of print]
PMID: 17113050

The main purpose of the present study was to determine
whether specific
regions of the mouse brain exhibit different age-related
changes in
oxidative stress, as indicated by glutathione redox state
and the level of
protein-glutathionyl mixed disulfides. Comparison of 3- and
21-month-old
mice indicated an age-related decrease in the ratio of
reduced to oxidized
glutathione (GSH/GSSG) as well as a pro-oxidizing shift in
the calculated
redox potential (ranging from 6 to 15 mV) in the cortex,
hippocampus,
striatum and cerebellum, whereas there was little change in
the brainstem.
This pro-oxidizing shift in redox state was due to a modest
decrease in GSH
content occurring in all the brain regions examined, and
elevations in GSSG
amount that were most pronounced in the striatum and
cerebellum. The
regional changes in glutathione redox state were paralleled
by increases in
the amounts of protein-mixed disulfides. A reduction of
caloric intake by
40% for a short period (7 weeks), implemented in relatively
old mice (17
months), increased the GSH/GSSG ratio and redox potential at
19 months in
the same brain regions that exhibited age-related decreases.
The effects of
age and caloric restriction were qualitatively similar in
C57BL/6 and DBA/2
mice. However, young DBA/2 mice, which do not show extension
of life span in
response to long-term caloric restriction, had lower
GSH/GSSG ratios and
higher protein-mixed disulfides than age-matched C57BL/6
mice. The current
findings demonstrate that oxidative stress, as reflected by
glutathione
redox state, increases in the aging brain in regions linked to
age-associated losses of function and neurodegenerative
diseases.