An Electrochemical Nanosensor Using a Screen-Printed Electrode Modified with 1T-MoS2/Nafion for Determination of Renin Inhibitor Aliskiren. Issue 1 (27th January 2021)

• Record Type: Journal Article
• Authors: Er, Engin; Erk, Nevin
• Is Part Of: Journal of the Electrochemical Society. Volume 168:Issue 1(2021)
• Publication Date: 2021-01-27
• Subjects: Molybdenum disulfide -- Modified electrode -- Electrochemical sensor -- Aliskiren -- Human plasma -- Determination; Electrochemistry -- Periodicals; 541.3705
• DOI: 10.1149/1945-7111/abdcc7
• Languages: English
• ISSNs: 0013-4651

Abstract

Abstract : An overdose of the antihypertensive agent in the human body causes a high cardiotoxicity, which may lead to the heart failure and stroke. The routine detection of amount of the antihypertensive agents in biological fluids is vital to control the regulation of blood pressure. In this work, a novel and sensitive electrochemical sensor based on nafion (NF) modified molybdenum disulfide in a metallic 1T phase (1T-MoS2 ) for voltammetric determination of renin-inhibitor Aliskiren (ALN) in human plasma. 1T-MoS2 was effectively synthesized by the exfoliation of bulk MoS2 using NaK alloy. The structure and morphology of 1T-MoS2 was characterized by Raman, XPS and TEM. The electrochemical behavior of ALN was investigated on a screen-printed electrode (SPE) modified with 1T-MoS2 /NF nanocomposite by cyclic voltammetry (CV) and adsorptive stripping differential pulse voltammetry (AdsDPV). The proposed electrochemical sensing platform (1T-MoS2 /NF/SPE) demonstrated a good electrochemical activity towards the ALN. Under optimized condition, 1T-MoS2 /NF/SPE exhibited an outstanding analytical performance for ALN with a wide linear working range of 0.05–7.0 μ M and a low limit of detection (LOD) of 8.0 nM. The reliability of the developed sensing platform was successfully tested by analyzing of ALN in human plasma samples with satisfactory recoveries. Therefore, 1T-MoS2 /NF/SPE could present as a promising analytical tool for the determination of ALN at trace level in clinical samples.