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PubMed2004

Plasmodium falciparum and the permeation pathway of the host red blood cell.

Invasion of red blood cells by malaria parasites leads to a huge increase in solute traffic across the membrane of a normally tight cell. Recent electrophysiological investigations strongly support earlier evidence from transport and pharmacological studies that the permeability pathway, which the parasite induces in the host cell membrane, is an anion-selective channel. This article analyzes the evidence and controversies concerning the nature of this channel, surveys the main open questions and suggests directions for future research in this area.

Animals↗
PubMed1996

Carboxylic ionophores in malaria chemotherapy: the effects of monensin and nigericin on Plasmodium falciparum in vitro and Plasmodium vinckei petteri in vivo.

Chloroquine is widely used in malaria chemotherapy. Due to its weak base properties, this drug accumulates in the parasite food vacuole where it acts initially by raising the pH of this organelle, thereby reducing the digestion of hemoglobin by the parasite and preventing its growth. Nevertheless, alkalinization of the food vacuole and inhibition of lysosomal protein degradation could also be achieved by means of carboxylic ionophores such as monensin and nigericin. These drugs intercalate into intracellular organelle membranes and exchange protons for K+ or Na+. In the present study, we show that monensin and nigericin exhibit in vitro intrinsic antimalarial activities at nanomolar and picomolar range, respectively, on P.falciparum and thereby appear 25 fold and 30,000 fold more potent than chloroquine. The very low IC50 values exhibited by these two ionophores prompted us to test their antimalarial activities in vivo on Plasmodium vinckei petteri. We found that the ED50 and ED90 values were respectively 1.1mg/kg and 3.5 mg/kg for monensin; 1.8 mg/kg and 4.6 mg/kg for nigericin. In addition, when treated with monensin at 10 mg/kg, 100% of the infected mice were cured. Interestingly, nigericin can be combined with monensin and we show that this combination is synergic. Thus, this finding would allow the use of lower doses of these ionophores and prevent occurrence of drug resistance. Carboxylic ionophores can be viewed as a new strategy in malaria chemotherapy.

Animals↗
PubMedDate not supplied

Highly pyrimethamine-resistant alleles of dihydrofolate reductase in isolates of Plasmodium falciparum from Tanzania.

In 2000 we used a sensitive technique to examine 9 isolates from malaria patients in Muheza, Tanzania who had failed treatment with sulfadoxine-pyrimethamine (SP). Three isolates carried, at low levels, the leucine to isoleucine change at amino acid 164 that is associated with clinical failure of SP. Numerous other highly resistant alleles were also observed.

Animals↗
PubMedDate not supplied

The effect of curdlan sulphate on development in vitro of Plasmodium falciparum.

Sulphated glycoconjugates have been reported to inhibit malarial merozoite invasion and interfere with rosetting and adhesion. Curdlan sulphate, a sulphated glycoconjugate with a favourable toxicity profile, exhibits antimalarial activity in vitro. The aim of this study was to characterize the antimalarial activity of curdlan and investigate its effect on adhesion. The antimalarial activity of curdlan at different points in the intraerythrocytic developmental cycle was investigated using morphological observation and radiolabelled hypoxanthine uptake as indices of parasite growth. Effects on adhesion were investigated using a platelet model. Curdlan suphate had no effect on the ability of the parasite to develop through the intraerythrocytic cycle. Inhibition of invasion was dependent on the drug being present at the time of invasion. Curdlan did not interfere with the ability of the parasite to adhere to the C36 receptor in the platelet model. In conclusion, the low toxicity of curdlan and its marked anti-invasion activity on merozoites make curdlan a potential auxiliary treatment for severe malaria.

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