Right now, let's just look
at an example of what happens
in terms of protein synthesis,
they kind of give this some reality.
So here we have a
bit of a membrane.
This would be rough
And on the surface of the
rough endoplasmic reticulum
is ribosome it's translating
its protein through
into the middle of the
looming of the rough ER.
Life is good,
except now we have ingested
or inhaled or done something
where we've gotten a fair little
high dose of carbon tetrachloride.
This is a compound used in dry
cleaning fluid, fairly common,
and we metabolize it in enzymes that
live in the endoplasmic reticulum.
In particular the cytochrome p-450
system, which is not a detoxifying system.
It is a solubilization system.
It's taking something
that's lipid soluble
and converting it to something
that is more water soluble,
so it could be excreted.
in that same endoplasmic reticulum,
takes our carbon tetrachloride
and converts it to carbon
trichloride with a free radical.
Oops, now we have a free radical in
the middle of a whole bunch of lipid.
What's gonna happen?
It can be predicted.
We're going to start in an autocatalytic
way, breaking down that entire membrane,
and we're getting more and
more and more free radicals
as because it's autocatalytic.
As we now break down the rest of
lipid, and the lipid is falling apart.
Our membrane is dissolving,
it's become a detergent.
When that happens,
our ribosome goes away.
It can't bind anymore,
so we're protein synthesis goes to zero.
Not so good.
Fortunately, we do know that we're
going to encounter things like this,
so we have ways to sup up,
to scavenge free radicals.
And vitamin E is one of those,
it lives in membranes in various places,
And it can be a free radical scavenger,
so it is a way to potentially stop this.
There are limits, you only have a certain
amount of vitamin E in your tissues,
so you cannot make infinite amounts of free
radicals and expect to get away with it.
But it is a mechanism by
which we protect ourselves.
And now there's some
by which we protect
ourselves from free radicals.
So here's the effect on
cellular activities and death.
If we look at our normal
rough endoplasmic reticulum,
and our normal mitochondria,
they have a certain structure and
architecture, and they look fine.
If we now hit them with a free radical,
in this case, carbon tetrachloride.
The ribosomes have left rough ER
and our mitochondria are swollen.
So we're not making protein
and we're not making ATP.
When that happens,
we will get cell death.
So this is on the right
hand side is a liver.
In an experimental animal that's
been exposed to carbon tetrachloride,
and we're getting these
areas of necrosis.
Cell death, cellular homicide and
those are pointed to with the arrows.