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Antidiabetic Drug Metformin Oxidation and in situ Interaction with dsDNA Using a dsDNA‐electrochemical Biosensor
Author(s) -
Machini W. B. S.,
Fernandes I. P. G.,
OliveiraBrett A. M.
Publication year - 2019
Publication title -
electroanalysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.574
H-Index - 128
eISSN - 1521-4109
pISSN - 1040-0397
DOI - 10.1002/elan.201900162
Subject(s) - electrochemistry , chemistry , detection limit , supporting electrolyte , redox , differential pulse voltammetry , nuclear chemistry , biosensor , electrode , cyclic voltammetry , inorganic chemistry , chromatography , biochemistry
The antidiabetic drug metformin (MET) is one of a group of emerging pharmaceutical drug contaminants in the wastewater treatment plants. The electrochemical behaviour of MET−Cu(II) complex by differential pulse and square wave voltammetry, in a wide pH range, at a glassy carbon electrode modified with a carbon black dihexadecylphosphate film (CB−DHP/GCE), was investigated. The MET−Cu(II) complex oxidation showed one pH‐dependent process, which leads to the formation of an oxidation product, being oxidized at a lower potential. The electroanalytical MET−Cu(II) complex detection limit, LOD=0.63 μM, and quantification limit, LOQ=2.09 μM, were obtained, and the MET−Cu(II) complex determination in wastewater samples collected from a senior residence effluent, using the CB−DHP/GCE, was achieved. Considering MET toxicity, the electrochemical evaluation of MET−dsDNA interaction, in incubated solutions and using dsDNA‐electrochemical biosensors, following the changes in the oxidation peaks of guanosine and adenosine residues electrochemical currents, was also investigated. The MET−dsDNA interaction mechanism, for shorter times, occurs by the binding of MET molecules in the minor grooves of the dsDNA, and for long times, the stabilization of the MET−dsDNA complex, causing a local distortion and/or unwinding of dsDNA morphology, is described. However, MET did not promote DNA oxidative damage.