Mitochondria oxidative damage?

Katharine Lindner katel at mv.mv.com
Fri Aug 2 01:16:06 EST 1996


mfossel at aol.com (MFossel) writes:

 
>Incidentally, I agree vis a vis mitochondria:  they are the major (95%)
>source of intracellular free radicals and therefore one of the major
>sources
>of entropic damage within cells.  The question is begged however (if we
>call
>them the only "cause" of aging) why have they been inherited flawlessly
>(for
>an estimate 1-2 billion years since they first took up residence in
>eukaryotic cells) and yet "age" within a matter of decades within your
>somatic cells?  What times (or switches on) this sudden degradation in
>function.  It clearly occurs in somatic cells (you are correct) and yet it
>clearly has not occurred within the inherited maternal germ cell line of
>mitochondria for an astounding timespan.  It is as though mitochondria are
>biologically immortal (and homeostatically flawless) for billions of years
>until you and I inherit them, and then go downhill almost instantly (in
>comparison).  This demands an explanation:  telomere theory, senescent
>gene
>expression, and cell senescence offers one that is consistant, elegant,
>and
>predictive.  So far (we'll see), this prediction has been borne out in the
>laboratory...

>
  Somewhere, I heard the idea that meiosis is a filter and cells with 
junk mitochondria get thrown away and other weak germ cells don't go on 
to become new animals.  So they start out with OK mitochondria.

  I don't know if this is right or wrong.

                                       Kathy




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