Abstract

Organophosphorus (OP) nerve agents are potent suicide inhibitors of the essential neurotransmitter-regulating enzyme acetylcholinesterase. Due to their acute toxicity, there is significant interest in developing effective countermeasures to OP poisoning. Here we impart nerve agent hydrolysis activity into the human drug metabolism enzyme carboxylesterase 1. Using crystal structures of the target enzyme in complex with nerve agent as a guide, a pair of histidine and glutamic acid residues were designed proximal to the enzyme's native catalytic triad. The resultant variant protein demonstrated significantly increased rates of reactivation following exposure to sarin, soman, and cyclosarin. Importantly, the addition of these residues did not alter the high affinity binding of nerve agents to this protein. Thus, using two amino acid substitutions, a novel enzyme was created that efficiently converted a group of hemisubstrates, compounds that can start but not complete a reaction cycle, into bona fide substrates. Such approaches may lead to novel countermeasures for nerve agent poisoning.

Highlights

  • Organophosphorus (OP) nerve agents are some of the most poisonous chemicals known (Figure 1A) [1]

  • Structure-Guided Dyad Design To hydrolyze the covalent phosphonyl-enzyme OP-bound species of Human carboxylesterase 1 (hCE1), we introduced a histidine (H) at position 146 and a glutamic acid (E) at position 363

  • The corresponding wild-type residues V146 and L363 are positioned on either side of the active site pocket, adjacent to the OP-serine bond formed during the twostep catalytic mechanism of the enzyme (Figure 2)

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Summary

Introduction

Organophosphorus (OP) nerve agents are some of the most poisonous chemicals known (Figure 1A) [1]. HCE1 is homologous in structure and catalytic mechanism to AChE and exhibits features that make it attractive as a potential nerve agent hydrolase [6]. Both hCE1 and AChE employ a catalytic triad consisting of serine, histidine, and glutamic acid residues. For both enzymes, OP nerve agents act as hemisubstrates – compounds that can start but not complete a reaction cycle to regenerate free active enzyme [7,8,9]. Wild-type (wt) hCE1 exhibits a slow hydrolysis-based reactivation after exposure to sarin, but no reactivation is observed when hCE1 is exposed to soman or cyclosarin [8]

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