Carbamate nerve agents reactivity

In the case of soman, therefore, once ageing has occurred, recovery of enzyme function depends on re-synthesis of AChE. As a result, it is important that an oxime is administered as soon after soman exposure as possible so that some reactivation of AChE occurs before all of the enzyme becomes aged. The phenomenon of soman-induced ageing led to the development of carbamate (pyridostigmine) prophylaxis for nerve agent poisoning. 

The carbamate anticholinesterases such as PB bind reversibly with ChE enzyme, yet spontaneously reactivate relatively rapidly. However, nerve agents (organophosphate compounds) bind with the ChE irreversibly and form a much more stable phosphory-lated enzyme (ChE-OP) complex. PB binds to peripheral ChE at anionic and esteratic sites and thus carbamylates the enzyme. The carbamylated enzyme sites cannot bind with nerve agents. In the meantime, some of the nerve agents are hydrolyzed to inactive metabolites by nonspecific hydrolases. The decarbamylation of the ChE takes place at the alcohol moiety on the esteratic site, regenerating the ChE enzyme to sustain life. 

First, carbamoylation, the interaction between carbamates and the active site of AChE, is freely and spontaneously reversible, unlike the normally irreversible inhibition of AChE by the nerve agents. No oxime reactivators are needed to dissociate, or decarbamoylate, the enzyme from a carbamate compound. Carbamates do not undergo the aging reaction of nerve agents bound to AChE. 

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