| Summary: | Nephrogenic diabetes insipidus (NDI), which can be congenital or acquired, results from the failure of the kidney to respond to the anti-diuretic hormone (ADH). This will lead to excessive water loss from the body in the form of urine. The kidney, therefore, has a crucial role in maintaining water balance and it is vital to restore this function in an artificial kidney. Herein, an ultrasensitive and highly selective aptameric graphene-based field-effect transistor (GFET) sensor for ADH detection was developed by directly immobilizing ADH-specific aptamer on a surface-modified suspended graphene channel. This direct immobilization of aptamer on the graphene surface is an attempt to mimic the functionality of collecting tube <inline-formula> <math display="inline"> <semantics> <mrow> <msub> <mi>V</mi> <mn>2</mn> </msub> </mrow> </semantics> </math> </inline-formula> receptors in the ADH biosensor. This aptamer was then used as a probe to capture ADH peptide at the sensing area which leads to changes in the concentration of charge carriers in the graphene channel. The biosensor shows a significant increment in the relative change of current ratio from 5.76 to 22.60 with the increase of ADH concentration ranging from 10 ag/mL to 1 pg/mL. The ADH biosensor thus exhibits a sensitivity of 50.00 µA·<inline-formula> <math display="inline"> <semantics> <mrow> <msup> <mrow> <mrow> <mo>(</mo> <mrow> <mi mathvariant="normal">g</mi> <mo>/</mo> <mi>mL</mi> </mrow> <mo>)</mo> </mrow> </mrow> <mrow> <mo>−</mo> <mn>1</mn> </mrow> </msup> </mrow> </semantics> </math> </inline-formula> with a limit of detection as low as 3.55 ag/mL. In specificity analysis, the ADH biosensor demonstrated a higher current value which is 338.64 µA for ADH-spiked in phosphate-buffered saline (PBS) and 557.89 µA for ADH-spiked in human serum in comparison with other biomolecules tested. This experimental evidence shows that the ADH biosensor is ultrasensitive and highly selective towards ADH in PBS buffer and ADH-spiked in human serum.
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