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 β-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 β-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.Free PDF Download
To cite this article
J.L. Imbert Palafox, L. González Linares, V.E. Reyes-Cruz, M.A. Becerril Flores, J.C. Ruvalcaba Ledezma, C.M. Gonzalez Alvarez, A. Arenas Flores, J.E. Bautista Garcia
In vitro redox activity of haemozoin and β-haemozoin interacting with the following antimalarials: artemether, lumefantrine and quinine
Eur Rev Med Pharmacol Sci
Vol. 24 - N. 12