Mitochondria oxidative damage?
dsc9w at avery.med.Virginia.EDU
Wed Jul 17 11:27:21 EST 1996
gmorley at hgmp.mrc.ac.uk writes:
> One theory I heard about the role of free radicals
> in the aging process mentioned that they can cause oxidative damage
> to the mitochondria.The argument went like this:
> All mitochondria in humans are of maternal origin -
> being passed down via the egg. New mitochondria are made
> only by other mitochondria - they are not encoded in the genome -
> and over time a higher proportion of dysfunctional ones are produced.
> I am not sure but I believe that like plasmids mitochondria have
> a copy number per cell.. thus eventually a large proportion of a cells
> resident mito. become defective. The resultant loss in energy output
> leads to general cellular damage, loss of skin elasticity and fatigue -
> aging in other words. This is not really my field so I was wondering
> about what other peoples reaction to this theory was?
> Personally I preffer telomeric shortening but I supose the two are
> not mutually exclusive. It might be interesting to translate the
> mitochondrial code into the genomic code (I believe there are differences)
> and engineer a mouse egg with the mitochondrail code intergrated
> into the genome.. it may be likely that the "error level correction"
> apparatus finds it more difficult to correct DNA mutations in mito
> than in the genome.(??) Does anyone have any ideas on this?
> Thanks (and be kind :))
> Gary Morley
> gmorley at rpms.ac.uk
Although I am not an expert on this, I do believe that
mitochondrial damage is integral to aging.
Most neurodegenerative diseases s involve damage to
mitochondria and increased free radical production.
There is evidence that mitochodrial mutations in the genes for
the electron transport chain are involved in the cell death in
Alzheimer's and Parkinson's disease (see recent papers by W.D.
Parker and M.F. Beal), which are not of course always a part of
aging, although clearly age-related.
As neurons are teminally differentiated, their aging and death
must involve mechanisms other than telomere loss. As the brain
is highly sensitive to oxidative damage and has relatively
lower levels of free-radical scavenging enzymes than other
tissues, mitochondrial dysfunction producing high amounts of
free radicals and hence damage and aging in the brain is very
plausible. It has already been demonstrated conclusively that
many rare neurodegenerative diseases are due to mitochondrial
mutations (MERRF, MELAS, Hereditary Optic Neuropathy or Leber's
Disease, Leigh's Disease, etc), and now the evidence that the
most common ND diseases like Alzheimer's and Parkinson's are
due to (or at least prominently involve) mitochondrial
pathology convinces me that mitochondria are clearly involved
somewhere in aging.
I think it's also interesting to note that Coenz Q, which
improves mitochondrial electron trans chain functioning (and
hence lessens free radical production) has been shown to extend
the life span of lab animals.
David S. Cassarino "The mind is not a vessel to be filled
MSTP, Neuroscience 2nd Year but a fire to be kindled."
UVA School of Medicine -Plutarch
dsc9w at virginia.edu
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