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According to the referenced papers, acetylcholinesterase that has been inhibited by an organophosphate possessing thiocholine as its leaving group is more susceptible to reactivation by oxime compounds compared to AChE inhibited by the neutral analogs of these compounds. One of the authors writes:

Sundwall (1961) reported that P2S was considerably more effective as an antagonist of the lethal action of 37 SN +(isopropoxy-2-trimethylammonio-tiomethylphosphino oxide) in mice than it was of those of Sarin and 37 S-N (isopropoxy-2-dimethylaminothiomethylphosphine oxide).

The author goes on to propose that the reason for this observation is that the phosphonyl group is oriented differently in AChE inhibited by the charged compound than in AChE inhibited by the neutral analog.

My question is: Is there any hard evidence that indicates that this proposed explanation is correct, such as crystallographic data? Are there any alternative possibilities?

References:

BOSKOVIC, B. (1981). The treatment of soman poisoning and its perspectives. Fundamental and Applied Toxicology, 1(2), 203–213. doi:10.1016/s0272-0590(81)80059-0

BošKović, B., Maksimović, M., & Minić, D. (1968). Ageing and reactivation of acetylcholinesterase inhibited with Soman and its thiocholine-like analogue. Biochemical Pharmacology, 17(8), 1738–1741. doi:10.1016/0006-2952(68)90237-2

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