Electrochemical oxidation of Fe (II) using chlorpromazine drug at boron-doped diamond electrode: application to in vivo mechanism study interaction of chlorpromazine on hemoglobin iron and evaluation of some biomolecules

Abstract

Abstract In this study, the electrochemical properties of aqueous chlorpromazine hydrochloride (CPZ) in the presence of Fe (II) were investigated by cyclic voltammetry at a boron-doped diamond (BDD) electrode. The results showed that an EC′ reaction mechanism occurs, where electrochemically generated CPZ species (cation radical) are reduced by Fe (II) back to the parent CPZ, and Fe (II) is oxidized to Fe (III). The detection limit, sensitivity, and dynamic concentration ranges were 2.8 μM, 0.0188 μA μM−1 and 10–166 μM. Based on the electrochemical results, the interaction of chlorpromazine (CPZ), a widely used antipsychotic tranquillizer, with the allosteric protein, hemoglobin, has been studied. First, four groups of six female rats weighing 400–450 g were selected. The rats were injected with different concentrations of chlorpromazine over a 3-week period, and the concentrations of hemoglobin, methemoglobin, red blood cells (RBCs), and hematocrit (HCT) were analyzed in the blood of each rat. After injection of different concentrations of the drug, the amount of hemoglobin) as a source of Fe (II)) decreased, but the amount of methemoglobin (as a source of Fe (III) increased. In addition, UV spectroscopic measurements in the range of 200–700 nm indicate the conversion of hemoglobin to methemoglobin in chlorpromazine-treated rats compared to the normal sample, and there was a direct relationship between the increasing methemoglobin concentration of chlorpromazine. Furthermore, the amount of RBC and HCT was measured. The results showed that RBC (21.05%–56.52%) and HCT (10.04%–53.19%) decreased. Finally, this study demonstrates a new mechanism for the effects of CPZ on hemoglobin iron in rat blood based on electrochemical results.