Garrett Jarboe

Case Study
1. The symptoms of each person are very similar. I would like to ask family
members if the deceased had all taken Tylenol. If so, when? Where was the
Tylenol purchased?
2. In my opinion these seven deaths are related. Due to the similar symptoms
and several of them taking Tylenol, I wonder if there is something wrong with
a batch of Tylenol that they all purchased.
1. These organs most likely lost the function of cellular respiration. This is
evident by the massive damage of the mitochondria which are major players
in cellular respiration.
2. This new information shows that there could have been a metabolism shut
down in the deceased. Hypoxia would shut down metabolism in these cells
because oxygen is needed to carry out cellular respiration in the
mitochondria. With the mitochondria not functioning this becomes more
possible for they are major hubs for metabolism and create energy. Without
energy these cells die and can lead to death once the organs can no longer
function. This data does not seem to be inconsistent.
1. Glucose is a substrate at the beginning of cellular respiration. It gets
broken down and forms pyruvates and electrons. Pyruvate then becomes
a substrate and is further broken down to release electrons. NAD+ is an
electron carrier which carries the electrons that were produced. NADH is
the product of this electron binding and carries the electrons to the
mitochondria for further steps of cellular respiration.
2. The NAD+ level is low while the NADH levels are extremely high. This is
most likely from the buildup of electrons in the mitochondria. This buildup
does not allow the NADH to drop off its electrons, which in turn, does not
allow the NADH to return to NAD+ form. The electron transport chain is
the most likely pathway effected.
3. This is because this part of cellular respiration is where the NADH and
electrons are used. This also so happens to be the place where O2 is
needed to remove the used electrons from the system by forming water.
With hypoxia, there would be no oxygen to be used in the electron
transport chain to remove electrons.
1. With cyanide being an inhibitor, CcOX could not function. The blockage of
CcOX would prevent the electron from completing the electron transport
chain and being bound to the O2.This would also block the passage of the
electron to the intermembrane space and being passed over the turbine.
This lack of turbine function would halt ATP production.
2. They died from hypoxia due to having no need to breath. With the
blockage of CcOX the electrons were unable to bind to O2. This created a
buildup of O2 in the mitochondria and blood stream and therefore no
breathing was necessary and they suffocated.
3. Artificial respiration most likely would not have worked because there was
no need to bring oxygen into the body. They had excess oxygen but were
just unable to use it. Even if they did do artificial respiration they most

likely would have died anyway from not having a functioning electron
transport chain to create energy.
4. The most likely source of the cyanide poisoning would be from the Tylenol.
Many of the deceased were reported of taking Tylenol and the rest
probably did too. They should look into what batch of Tylenol the deceased
took. The police should then create an immediate recall of the Tylenol
batch. They should notify the public of the danger and remove the tainted
Tylenol from store shelves.