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now let's take a look at summarizing
some of the things that happen with
mitochondrial dysfunction what's going
on in our mitochondria we know that they
are especially prone to DNA damage and
there's even a whole theory the
mitochondrial free radical theory that
suggests that the more we consume and
eat the more cell respiration that goes
on and thus the more oxygen is split in
order to form h2o right which generates
when we split the oxygen free radicals
that can go around and do damage and the
more of that damage that's done the more
agent cells become now there have been
some challenges to this free radical
theory or expounding upon that three
free radical theory it really depends on
how you look at it but this is how I
would summarize that information so it
turns out that not only do we have the
idea that yes indeed by toq Andreea do
accumulate free radical damage
throughout their lifetime and that
becomes more with aging but is it purely
because of the increase in free radicals
or oxidative reactive oxygen species so
the question is do these species
actually cause our deterioration or what
else might be going on so more recent
evidence suggests that perhaps the
mitochondria in response to stress right
if they're not functioning that well or
if there's not enough energy around we
would up regulate the production of
mitochondria such that there are many
more mitochondria and in has a
consequence of that the more
mitochondria are producing more reactive
oxygen species or one half oh twos that
are able to go around and do more damage
but we are also increasing the energy
output so that
my counteract that anyway so we are in
as a congruent thing we are growing more
mitochondria in each cell and they are
also producing more reactive oxygen
species and so perhaps the increase in
reactive oxidant species or Ross is due
to the fact that there are simply more
mitochondria either way the reactive
oxygen species are causing damage and
are certainly aligned with cellular
aging so just a little note on some of
the newer research but free radical
Theory is sort of the leading idea at
the moment moving on to the next
physiological trait of aging you are
probably very familiar with the idea of
telomere attrition certainly we have
covered that telomeres shorten as cells
go through divisions and stem cells and
cancer cells might have telomerase
active and so they can continue to grow
or regenerate telomeres however most
somatic cells lose that capacity and
you're probably familiar with the
hayflick limit hayflick limit suggests
that there are a limited number of cell
divisions that somatic cells can go
through before the telomeres become
short enough to start doing damage to
the I guess sub telomeric regions of the
chromosome
once the telomeres have essentially run
out it suggested that 50 divisions is
about the maximum for any somatic cell
so after that each cell division is
shortening the ends of the chromosomes
till we start actually nibbling away at
the genes located on the ends of the
chromosomes which as you can imagine can
have some manifestations in the
condition of the cell so telomeric
attrition definitely
associated with the aging cell
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