First of all, for various reasons (more on this later), he must not be poisoned right away, but instead pretend to be dead (the widow never checks his pulse). Then the widow pushed him and the other corpses into the asphalt pool. Since the sinking speed was very slow in the asphalt, he climbed out again after the widow left; or the widow ran away without caring about the corpse because she found that the money had been left behind.
In short, as long as he lives until the widow leaves, nothing will happen.
It has been said that "one of the mechanisms by which thallium is lethal is that 'thallium inhibits acetylcholinesterase, the enzyme that breaks down the neurotransmitter acetylcholine specifically mentioned in the tablet. Acetylcholine accumulation in excess can lead to severe toxicity. He is deficient in acetylcholine. , so this inhibition of acetylcholinesterase won't cause as much damage.'"
We should have all learned in high school biology class that neurotransmitters are released from the presynaptic membrane, which is linked to the postsynaptic membrane. The binding of the receptors changes the permeability of the membrane, changes the potential of the posterior membrane, and conducts nerve impulses. The neurotransmitter is generally decomposed by the corresponding enzyme immediately after binding to the receptor, otherwise it will continue to generate nerve impulses.
Regarding acetylcholine, what I found is:
the relationship between acetylcholine and human Parkinson's disease
Parkinson's disease, also known as "tremor palsy", is a degenerative disease of the central nervous system, mainly due to the After the pathological changes in cells, the synthesis of dopamine is reduced, the function of inhibiting acetylcholine is reduced, and the excitatory effect of acetylcholine is relatively enhanced. The result of the imbalance between the two is "tremor palsy".
It can be seen from this that if acetylcholine is not decomposed in time, it will produce convulsions similar to Parkinson's.
So why is acetylcholine not decomposed in time after thallium poisoning? People say that it is because the acetylcholinesterase that decomposes it is inhibited by thallium.
In the toxicity mechanism of thallium, we can search for:
Thallium ions combine with sulfhydryl groups in proteins, resulting in the loss of physiological activity. It is currently known that thallium binds to related proteins in mitochondria, resulting in uncoupling of oxidative phosphorylation and interfering with the body's energy metabolism; thallium also binds with sulfhydryl groups in keratin. Combined, affects the synthesis of keratin, leading to hair loss and the production of Mie lines.
I don't know if there is a sulfhydryl group (-SH) in acetylcholinesterase, but it is a macromolecular protein after all, and it is likely to contain it; even if it does not, it may be interfered, which needs further research.
If it is true that acetylcholinesterase can be inhibited by thallium, then Charlie, who lacks acetylcholine in the first place, will not have such severe convulsions, then he can easily escape the asphalt pool, wait until he gets home, and then take a detoxification such as pulan, and his survival goal is achieved. !
Incidentally, thallium poisoning is divided into acute and chronic, and the widow's alcohol must be acute. So why did the widow use the poison for so long, but did not find that thallium poisoning took a long time to kill, it is very likely that the drinker was in a state of convulsions, which made her mistakenly think that the person was dead at that time (not to mention her Never confirming whether a person is dead or not), he just walked away.
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