Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21202, United States.
Department of Chemistry, Texas A&M University, College Station, Texas 77842, United States.
Langmuir. 2021 May 4;37(17):5213-5221. doi: 10.1021/acs.langmuir.1c00166. Epub 2021 Apr 20.
Electrochemical aptamer-based (E-AB) sensors are a technology capable of real-time monitoring of drug concentrations directly in the body. These sensors achieve their selectivity from surface-attached aptamers, which alter their conformation upon target binding, thereby causing a change in electron transfer kinetics between aptamer-bound redox reporters and the electrode surface. Because, in theory, aptamers can be selected for nearly any target of interest, E-AB sensors have far-reaching potential for diagnostic and biomedical applications. However, a remaining critical weakness in the platform lies in the time-dependent, spontaneous degradation of the bioelectronic interface. This progressive degradation-seen in part as a continuous drop in faradaic current from aptamer-attached redox reporters-limits the in vivo operational life of E-AB sensors to less than 12 h, prohibiting their long-term application for continuous molecular monitoring in humans. In this work, we study the effects of nuclease action on the signaling lifetime of E-AB sensors, to determine whether the progressive signal loss is caused by hydrolysis of DNA aptamers and thus the loss of signaling moieties from the sensor surface. We continuously interrogate sensors deployed in several undiluted biological fluids at 37 °C and inject nuclease to reach physiologically relevant concentrations. By employing both naturally occurring d-DNA and the nuclease-resistant enantiomer l-DNA, we determine that within the current lifespan of state-of-the-art E-AB sensors, nuclease hydrolysis is not the dominant cause of sensor signal loss under the conditions we tested. Instead, signal loss is driven primarily by the loss of monolayer elements-both blocking alkanethiol and aptamer monolayers-from the electrode surface. While use of l-DNA aptamers may extend the E-AB operational life in the long term, the critical issue of passive monolayer loss must be addressed before those effects can be seen.
基于电化学适体的 (E-AB) 传感器是一种能够实时监测体内药物浓度的技术。这些传感器通过附着在表面的适体实现其选择性,这些适体在与靶标结合时改变其构象,从而导致与电极表面结合的适体结合的氧化还原报告分子之间的电子转移动力学发生变化。由于理论上可以为几乎任何感兴趣的靶标选择适体,因此 E-AB 传感器在诊断和生物医学应用方面具有广泛的应用前景。然而,该平台仍然存在一个关键的弱点,即生物电子界面的时间依赖性自发降解。这种渐进的降解——部分表现为附着在适体上的氧化还原报告分子的法拉第电流持续下降——限制了 E-AB 传感器在体内的工作寿命,使其在体内的操作寿命不到 12 小时,从而禁止其用于人类的长期连续分子监测。在这项工作中,我们研究了核酸酶作用对 E-AB 传感器信号寿命的影响,以确定信号的逐渐损失是否是由于 DNA 适体的水解,从而导致传感器表面的信号部分丢失。我们连续在 37°C 的几种未稀释的生物流体中检测传感器,并注入核酸酶以达到生理相关的浓度。通过使用天然存在的 d-DNA 和对核酸酶有抗性的对映体 l-DNA,我们确定在当前最先进的 E-AB 传感器的寿命内,在我们测试的条件下,核酸酶水解不是传感器信号损失的主要原因。相反,信号损失主要是由电极表面的单层元素——包括阻塞烷硫醇和适体单层——的损失驱动的。虽然使用 l-DNA 适体可能会在长期内延长 E-AB 的工作寿命,但在看到这些效果之前,必须解决被动单层损失的关键问题。