The effect of two anionic membranes (AMI 7001s and Neosepta AMX) on the electrodeposition of manganese from sulphate solutions.

The effect of two different anionic membranes on manganese deposition was studied in a two-compartment electrochemical reactor with a titanium cathode and a dimensionally stable RuO2|Ti anode. Chronopotentiometry, ICP-OES, SEM, XRD and elemental mapping were used to understand the changes in concentration and characteristics of the metallic deposition at different current densities with the anionic membranes AMI 7001s and Neosepta AMX. The results demonstrate that AMI reduces more manganese than AMX below -100 A m-2, generating more metallic deposition but also more low-solubility manganous by-products, whereas both membranes exhibited similar behaviours above -100 A m-2 reaching the maximum current efficiency (63%) at -200 A m-2. It was also observed that the membranes have a significant effect on sulphate consumption since they are anions.

Selenium and sulphur reactions involved in manganese reduction from sulphate solutions.

Electrochemical reduction of ionic species during manganese deposition from sulphated aqueous solutions has been studied in an electrochemical reactor with two anionic exchange membranes. Thermodynamic analysis, voltammetries, and chronopotentiometries were used to determine the reaction mechanism of the reductions developed, with the results demonstrating that the effect of the elemental selenium on the hydrogen evolution leads to the formation of elemental sulphur by reducing the sulphate ions with both membranes. It was also evident that in the range of -25 to -50 A m-2 the electrodeposition of metallic manganese begins, with minimal interference from parasitic reactions.

In vitro redox activity of haemozoin and ß-haemozoin interacting with the following antimalarials: artemether, lumefantrine and quinine.

OBJECTIVE: Malaria parasites invade, grow and multiply inside erythrocytes and obtain nourishment from haemoglobin. Then, the released haem group is oxidized to haematin and inert dimeric haemozoin bio-crystals form, which provides the parasite a unique way to avoid the toxicity associated with the haem group. Therefore, antimalarial drugs are designed to inhibit dimer formation; however, recent electrochemical studies indicate that an inert dimer also promotes a toxic oxidizing environment. Therefore, this work explores drug reactivity in the presence of monomers and dimers to evaluate their contribution to redox activity. MATERIALS AND METHODS: Three medicines mixed with haemozoin or ß-haemozoin in carbon paste electrodes were tested using cyclic voltammetry. RESULTS: The data indicated again that the substances modify the natural redox state of haemozoin and ß-haemozoin. This effect could be attributed to the natural oxidation potential of the drugs. In addition, it was found that the oxidation potential decreased through quinine, lumefantrine and artemether with the same tendency in the presence of haemozoin but with less current density. Additionally, it was observed that the oxidation response between the monomer haemozoin and antimalarial drugs is carried out at more negative potentials. CONCLUSIONS: Together, the total results indicate that antimalarials per se can contribute to oxidation processes and that in combination with monomeric or dimeric haemozoin can increase or decrease the oxidizing power of the haemozoin forms. The various oxidizing environments suggest that the cell membranes can also be damaged by the unique presence of the antimalarial.