Abstract

Solid-phase synthesis is an elegant way to create molecularly imprinted polymer nanoparticles (nano-MIPs) comprising a single binding site, i.e. mimics of antibodies. When using human serum albumin (HSA) as the template, one achieves nano-MIPs with 53 ± 19 nm diameter, while non-imprinted polymer nanoparticles (nano-NIPs) reach 191 ± 96 nm. Fluorescence assays lead to Stern–Volmer plots revealing selective binding to HSA with selectivity factors of 1.2 compared to bovine serum albumin (BSA), 1.9 for lysozyme, and 4.1 for pepsin. Direct quartz crystal microbalance (QCM) assays confirm these results: nano-MIPs bind to HSA immobilized on QCM surfaces. This opens the way for competitive QCM-based assays for HSA: adding HSA to nanoparticle solutions indeed reduces binding to the QCM surfaces in a concentration-dependent manner. They achieve a limit of detection (LoD) of 80 nM and a limit of quantification (LoQ) of 244 nM. Furthermore, the assay shows recovery rates around 100% for HSA even in the presence of competing analytes.

Highlights

  • Human serum albumin (HSA) contains 585 amino acids and is widely known as the most abundant protein in the human body, at concentrations of approximately 3.5–5 g/dL

  • Abnormal levels are indicative of health problems: increased HSA levels— so-called hyperalbuminemia—are usually associated with a protein-rich diet combined with a high level of exercise [3]

  • The level of HSA is a marker of liver function; low HSA concentration—called hypoalbuminemia—is often a consequence of cirrhosis [2, 4]

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Summary

Introduction

Human serum albumin (HSA) contains 585 amino acids and is widely known as the most abundant protein in the human body, at concentrations of approximately 3.5–5 g/dL. It plays important roles in body metabolism including metabolite delivery, enzymatic activity, plasma oncotic pressure regulation, and antioxidant properties [1, 2]. In the same way, decreased HSA levels are warning signals: for example, chronic liver diseases with hepatocyte malfunction reduce HSA synthesis. The level of HSA is a marker of liver function; low HSA concentration—called hypoalbuminemia—is often a consequence of cirrhosis [2, 4]. Decreasing HSA levels correlate with the Published in the topical collection celebrating ABCs 20th Anniversary

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