No quintessentially british James bond film is complete without the inevitable cyanide poisoining. A vial filled with a sinister red liquid? Maybe a stereotypical red and white capsule?
Neither actually. It’s relatively blue to be fair.
Cyanide is, without doubt, one of the deadliest poisons out there. Its ways of working in a creative yet ominous manner are what lead it to be one of the most well-known and discussed toxins in the world.
To understand the true extent to which cyanide is able to have such an unalterable affect is to reduce it down to a couple of cells and chemicals. Enzymes, to be precise — what I would consider the most fascinating biological molecules to exist. Their diversity and functionality is so variable that there is a whole separate branch of biomedicine dedicated to it.
If we boil cyanide down to an enzyme and a substrate reaction, cyanide is what we would consider a non-competetive inhibitor. A non-competetive inhibitor is a molecule which attaches itself to the allosteric binding site of an enzyme. The allosteric binding site is not the main active site where the enzyme-substrate complex forms, but is rather another area on the enzyme which can effectively form bonds with another molecular substance due to the chemical properites of the amino acids in that region.
Non- competetive inhibitors are the sneaky ones. By attaching to the binding site they trigger a conformational shape change in the enzyme. This change in shape has a ripple effect, altering everything up to the active site itself. Now let’s bring ourselves back to GCSE biology: the active site of an enzyme determines its function, changing the active site or a denaturing of the active site will result in a non-functional enzyme.
This is the most fundamental theory of biochemistry.
Cyanide is a chemical compund involving the CN⁻ anion, with its most toxic forms being the compounds of potassium and sodium.
2,6-dimethyloxybenzoyl cyanide (note the c-n chain suggesting the cyanide group)
Cyanide can normally be found in several safe to eat foods including almonds, lima beans, soy and spinach.
These aren’t particulary poisonous because their ingestion does not trigger the release of the CN⁻ ion. This ion is the inhibitor to the transmembrane protein- cytochrome c oxidase (COX) — which is responsible for one of the final stages of respiration, namingly oxidative phosphorylation. Cyanide binds to the haem group within COX and prevents electrons passing through the protein to the oxygen molecules which not only blocks the mitochondrial transport chain, but also interferes with the pumping out of a proton from the mitochondrial matrix. It therefore not only inhibits aerobic respiration, but also the synthesis of ATP.
diagram depicting the inner and outer membrane of a mitochondria — the electron transport cycle is shown.
The result:
Instant death.
But “instant death” puts it lightly. More precisely speaking: apnea, seizures, pulmonary edema and cardiac arrest, resulting in a persistent vegetative state.
I spent a while trying to figure out how I might end this on a high note, possibly drift away from the slightly depressing thought of being poisoned with cyanide, but no idea immediately sprang to mind. So instead, you’ve gained a newfound love for enzymes and proteins and maybe you’ll admire the complexity of the human body as much as I do.