Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, 789 South Limestone Street, Lexington, Kentucky 40536, USA.
J Phys Chem B. 2011 May 5;115(17):5017-25. doi: 10.1021/jp200975v. Epub 2011 Apr 12.
First-principles quantum mechanical/molecular mechanical free energy calculations have been performed to examine the catalytic mechanism for cocaine esterase (CocE)-catalyzed hydrolysis of (+)-cocaine in comparison with CocE-catalyzed hydrolysis of (-)-cocaine. It has been shown that the acylation of (+)-cocaine consists of nucleophilic attack of the hydroxyl group of Ser117 on the carbonyl carbon of (+)-cocaine benzoyl ester and the dissociation of (+)-cocaine benzoyl ester. The first reaction step of deacylation of (+)-cocaine, which is identical to that of (-)-cocaine, is rate-determining, indicating that CocE-catalyzed hydrolyses of (+)- and (-)-cocaine have a common rate-determining step. The computational results predict that the catalytic rate constant of CocE against (+)-cocaine should be the same as that of CocE against (-)-cocaine, in contrast with the remarkable difference between human butyrylcholinesterase-catalyzed hydrolyses of (+)- and (-)-cocaine. The prediction has been confirmed by experimental kinetic analysis on CocE-catalyzed hydrolysis of (+)-cocaine in comparison with CocE-catalyzed hydrolysis of (-)-cocaine. The determined common rate-determining step indicates that rational design of a high-activity mutant of CocE should be focused on the first reaction step of the deacylation. Furthermore, the obtained mechanistic insights into the detailed differences in the acylation between the (+)- and (-)-cocaine hydrolyses provide indirect clues for rational design of amino acid mutations that could more favorably stabilize the rate-determining transition state in the deacylation and, thus, improve the catalytic activity of CocE. This study provides a valuable mechanistic base for rational design of an improved esterase for therapeutic treatment of cocaine abuse.
已进行了第一性原理量子力学/分子力学自由能计算,以研究可卡因酯酶 (CocE) 催化 (+)-可卡因水解的催化机制,并与 CocE 催化 (-)-可卡因水解进行了比较。结果表明,(+)-可卡因的酰化反应包括 Ser117 上的羟基对 (+)-可卡因苯甲酰酯的羰基碳原子的亲核攻击和 (+)-可卡因苯甲酰酯的解离。(+)-可卡因去酰化的第一步反应与 (-)-可卡因相同,是速率决定步骤,表明 CocE 催化 (+)-和 (-)-可卡因的水解具有共同的速率决定步骤。计算结果预测,CocE 对 (+)-可卡因的催化速率常数应该与 CocE 对 (-)-可卡因的相同,这与人类丁酰胆碱酯酶催化 (+)-和 (-)-可卡因水解之间的显著差异形成对比。通过比较 CocE 催化 (+)-可卡因水解与 CocE 催化 (-)-可卡因水解的实验动力学分析,证实了这一预测。确定的共同速率决定步骤表明,CocE 高效突变体的合理设计应集中在去酰化的第一步反应上。此外,获得的酰化反应中 (+)-和 (-)-可卡因之间详细差异的机制见解为合理设计氨基酸突变提供了间接线索,这些突变可以更有利于稳定去酰化过程中的速率决定过渡态,从而提高 CocE 的催化活性。这项研究为合理设计用于治疗可卡因滥用的改良酯酶提供了有价值的机制基础。