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.
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. Thus, the more oxygen is split
in order to form H2O which generates when we split the oxygen free radicals that can go around
and do damage. The more of that damage that’s done, the more aged cells become.
Now, there have been some challenges to this free radical theory or expounding upon
that free radical theory. It really depends on how you look at it. But this is how I would summarize
that information. It turns out that not only do we have the idea that yes indeed, mitochondria 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?
More recent evidence suggests that perhaps the mitochondria, in response to stress,
if they’re not functioning that well or if there’s not enough energy around, we would upregulate
the production of mitochondria such that there are many more mitochondria. As a consequence of that,
the more mitochondria are producing more reactive oxygen species or ½ O2s that are able to go around
and do more damage, but we are also increasing the energy output so that might counteract that.
Anyway, as a congruent thing, we are growing more mitochondria in each cell. They are also producing
more reactive oxygen species. So, perhaps the increase in reactive oxygen species or ROS
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. Stem cells and cancer cells might have telomerase active.
So, they can continue to grow or regenerate telomeres. However, most somatic cells lose that capacity.
You’re probably familiar with the Hayflick limit. Hayflick limit suggests that 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, subtelomeric regions of the chromosome once the telomeres
have essentially run out. It's suggested that 50 divisions is about the maximum for any somatic cells.
After that, each cell division is shortening the ends of the chromosomes until 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.