On Biomimetics by Lilyana Pramatarova

(lily) #1

On Biomimetics
388


was actually known about the milieu in which it was formed in vivo, or about its
mechanism of formation until 2005. The last six years have seen major strides towards
answering both of these questions. We now know that haemozoin formation is intimately
associated with lipid-droplet like structures in both Plasmodium and Schistosoma, and with
lipid vesicle bilayers in Rhodnius. At least in Plasmodium, these are now known to be neutral
mono- and diacylglycerols. Biomimetic investigations using solvent interfaces and SNLDs
have shown that interfaces between aqueous and non-aqueous media are extraordinarily
active in promoting formation of the synthetic counterpart of haemozoin, -haematin. In
terms of reaction rates, they far exceed any other known process of -haematin formation.
Surface-sensitive measurements, specifically using GIXD and XR of -haematin formed at
such surfaces, and even more convincingly XR of crystals nucleated on SAMs strongly point
to lattice epitaxy being the mechanism by which these surfaces mediate the process. These
techniques provide a platform for further investigation. For example, what effects do
various constituents of the digestive vacuole of the malaria parasite, such as ions and globin
fragments have on the reaction rate? What role do proteins play in the process, either in
chaperoning haem to the lipid surface and preventing it from precipitating as amorphous
haematin, or in directly accelerating the process of haemozoin formation in conjunction with
lipids? How do drugs such as chloroquine inhibit haemozoin formation? It is likely that
with the methods and techniques now available, many of these questions will be able to be
answered.



  1. Acknowledgements


The National Research Foundation of South Africa is acknowledged for financial support.
Any opinion, findings and conclusions or recommendations expressed in this material are
solely those of the author.



  1. References


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