Cytochrome a3, the third and final active site of the cytochrome c oxidase complex, actually contains both iron and copper (as Fe(II) and Cu(I) in the reduced, ‘resting’ complex and Fe(III) and Cu(II) in the oxidized complex). In normal activity, this binding site is geometrically optimal for a molecule of O2 to slide into the gap between the iron atom (which is bound by a large, planar heme-a ligand) and the copper atom (bound to three histidine residues from the protein it’s contained in, if you want to know…). The oxygen molecule binds to both the Fe and the Cu, and then undergoes the final reaction of “cellular respiration”:
O2 + 8 H+ + 4 e- --> 2 H2O + 4 H+
The significance is that those four protons on the right side are in a different place than the ones on the left – they’ve been transported across the mitochondrial membrane, and they can now be used to synthesize ATP.
Cyanide works by binding to cytochrome a3, as Mycroft explained. It does so much better than O2 can – it’s exactly the right size, and its electronic properties are much better for binding (for reasons I won’t get into…) than oxygen is. (Incidentally, the carbon atom is closer to the iron atom, and the nitrogen closer to the copper; the binding is linear.) The binding is irreversible, and so ATP synthesis rapidly stops. This doesn’t just kill by preventing the heart from beating; it also prevents nerves from functioning. I expect that cyanide poisoning, with sufficient concentration, causes rapid loss of consciousness. If ‘death’ is defined as the cessation of ATP synthesis, then cyanide poisoning would be one of the most rapid mechanisms of causing death.
Amyl nitrite (or any alkyl nitrite) has to be given immediately after exposure to cyanide, since it doesn’t reverse the effects of cyanide poisoning. It works by oxidizing the Fe(II) in hemoglobin to Fe(III) to form methemoglobin; cyanide reacts with methemoglobin to form cyanomethemoglobin, which is not capable of transporting oxygen but not toxic either. (I was also told that it oxidizes cyanide to cyanate, but that’s not what the monograph (PDF) for sodium nitrite says.
Some other poisons:
Carbon monoxide binds irreversibly to hemoglobin to form carboxyhemoglobin; it would kill more slowly than CN, because it doesn’t act as directly.
Arsenic is most toxic as arsenite, As(III). Arsenic poisoning is typical heavy-metal poisoning; generally chronic exposure is required to kill (though massive doses can kill quickly), which is why it’s such a good mystery-novel poison. It works by binding to the -SH (sulfhydryl) groups of cysteine residues in proteins. Hair contains a lot of these, which is why arsenic poisoning can be detected from hair samples. It also subsitutes for phosphorus in bones. Mercury also has a high affinity for sulfur and works much the same way as arsenic. Mercury metal is not toxic, but its vapor is dangerous, and all compounds of mercury are dangerous, some in milligram quantities.
Acetylcholinergic poisons: Curare is an antagonist (blocker)at the nicotinic acetylcholine receptor, which is important for skeletal muscle function. I assume that it paralyzes the victim, but leaves their brain functioning until they lose consciousness due to heart failure. Sarin, Tabun, VX, and similar nerve gases do the opposite – they overload acetylcholine receptors by blocking the enzyme that breaks the neurotransmitter down. (I suppose that curare, in small doses, could work like atropine as an antidote for these agents…) Strychnine acts at a different site, the glycine receptor, also as an antagonist.