Midwest Center for Structural Genomics and Structural Biology Center, Biosciences, Argonne National Laboratory, Argonne, IL 60439, USA.
FASEB J. 2013 May;27(5):1917-27. doi: 10.1096/fj.12-224014. Epub 2013 Jan 30.
The specter of a return to an era in which infectious disease looms as a significant threat to human health is not just hyperbole; there are serious concerns about the widespread overuse and misuse of antibiotics contributing to increased antibiotic resistance in pathogens. The recent discovery of a new enzyme, first identified in Klebsiella pneumoniae from a patient from New Delhi and denoted as NDM-1, represents an example of extreme promiscuity: It hydrolyzes and inactivates nearly all known β-lactam-based antibiotics with startling efficiency. NDM-1 can utilize different metal cofactors and seems to exploit an alternative mechanism based on the reaction conditions. Here we report the results of a combined experimental and theoretical study that examines the substrate, metal binding, and catalytic mechanism of the enzyme. We utilize structures obtained through X-ray crystallography, biochemical assays, and numerical simulation to construct a model of the enzyme catalytic pathway. The NDM-1 enzyme interacts with the substrate solely through zinc, or other metals, bound in the active site, explaining the observed lack of specificity against a broad range of β-lactam antibiotic agents. The zinc ions also serve to activate a water molecule that hydrolyzes the β-lactam ring through a proton shuttle.
传染病再次成为严重威胁人类健康的重大威胁,这种情况一去不复返,这种说法并非危言耸听;人们严重担忧抗生素的广泛过度使用和滥用会导致病原体对抗生素的耐药性增加。最近发现了一种新的酶,最初在来自新德里的患者的肺炎克雷伯菌中发现,并被命名为 NDM-1,它代表了极端混杂的一个例子:它以惊人的效率水解并使几乎所有已知的基于β-内酰胺的抗生素失活。NDM-1 可以利用不同的金属辅因子,并且似乎利用基于反应条件的替代机制。在这里,我们报告了一项结合实验和理论研究的结果,该研究检查了酶的底物、金属结合和催化机制。我们利用通过 X 射线晶体学、生化测定和数值模拟获得的结构来构建酶催化途径的模型。NDM-1 酶仅通过锌或结合在活性部位的其他金属与底物相互作用,这解释了对广泛的β-内酰胺抗生素药物缺乏特异性的观察结果。锌离子还可以激活水分子,通过质子转移水解β-内酰胺环。