Bad Mitochondria May Actually Be Good For You

ScienceDaily (July 23, 2009) — Mice with a defective mitochondrial
protein called MCLK1 produce elevated amounts of reactive oxygen when
young; that should spell disaster, yet according to a study in this
week's JBC these mice actually age at a slower rate and live longer
than normal mice.

Mitochondrial oxidative stress is a popular theory explaining the
aging process; over time, reactive oxygen species produced by
mitochondria while they make energy slowly accumulate and begin
damaging cells, including the mitochondria. Several recent studies
have begun to question this theory, though, and to get some more
direct answers, Siegfried Hekimi and colleagues at McGill University
examined the mitochondria of MCLK1-defective mice, a strain known for
its longevity, at various ages.

What they found was that in young (3 month old) MCLK1-defective mice,
mitochondria were quite energy inefficient and produced a lot of
harmful oxygen radicals; yet surprisingly, when these mice were 23
months old, their mitochondria were working better than normal mice.
So, despite the oxidative stress, these mice experienced less
deterioration than normal.

To confirm whether MCLK1-defiency could be somehow protective, the
researchers crossed MCLK1-defective mice with those lacking SOD2, a
major protein antioxidant. Normally, SOD2-defective mice accumulate
cellular damage quickly, yet when combined with MCLK1-defiency, they
exhibited less damage and oxidative stress.

In explaining this seeming paradox, Hekimi and colleagues suggest that
while MCLK1-defective mice produce more oxygen radicals from their
mitochondria, their overall inefficiency results in less energy and
fewer oxygen radicals being produced in other parts of a cell. Thus
while these mice may have some higher risks of damage while young,
they accumulate less damage as they age –a finding that seems to
indicate the mitochondrial stress theory may not be correct.

http://www.sciencedaily.com/releases/2009/07/090722123753.htm

-----------------------------

Could this ROS overproducing mitochondria ultimately destroy the aging
program in the brain?  Or is it just plain hormesis?

Taka