The malaria parasite, Plasmodium falciparum, detoxifies heme generated from digestion of its host's blood by coalescing the toxin into a harmless crystal.

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Mosquitoes are responsible for spreading malaria, a protozoan disease that kills nearly one million people annually. But the risk actually runs both ways. That is, every time the mosquito bites its victim, it puts itself at risk from exposure to the iron-containing part of red blood cells, called heme, which is generated as a byproduct of blood digestion and toxic to the mosquito. The parasite, Plasmodium falciparum, sidesteps toxic exposure by binding free hemes together into an insoluble crystal structure. It does so by forming microscopic drops of oil into which free heme self assembles into crystal pairs (dimers) which then coalesce into non-toxic hemozoin crystals.

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"How exactly aqueous heme is removed from the acidic digestive vacuolar solution [of the malaria parasite Plasmodium falciparum] and converted into harmless hemozoin in order to avert membrane lysis, lipid peroxidation and inevitable parasite destruction has been the subject of much debate and previous reviews." (Pisciotta and Sullivan 2008:4)

"Lipid droplets catalyze the biomineralization of heme to hemozoin by concentrating lipophilic heme from the aqueous environment in which hemoglobin digestion transpires. The exclusion of water facilitates heme’s transition from the aqueous dimer to the iron (III)--carboxylate heme crystal dimer. Inside the non-polar, hydrophobic microenvironment of the lipid droplet individual heme crystal dimers then integrate via hydrogen bonding into the growing face of the hemozoin crystal." (Pisciotta and Sullivan 2008:6)

"The site of lipid heme crystallization has important implications for drug inhibition...higher lipophilicity constants amongst a diverse set of quinolines was correlated with lower inhibitory concentrations against chloroquine-resistant parasites." (Pisciotta and Sullivan 2008:5)

Journal article
Hemozoin: Oil versus waterParasitology InternationalNovember 20, 2007
John M. Pisciotta, David Sullivan

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