| ironjustice@aol.com 2006-10-02, 8:28 am |
| Public release date: 29-Sep-2006
Contact: Katarina Sternudd
katarina.sternudd@ki.se
46-852-483-895
Karolinska Institutet
New treatment for severe malaria
The most dangerous form of malaria is difficult to treat and claims two
million lives a year. Now, researchers at Karolinska Institutet in
Sweden have developed a powerful new weapon against the disease.
Severe anaemia, respiratory problems and encephalopathy are common and
life-threatening consequences of serious malaria infection. The
diseases are caused when the malaria bacteria P.falciparium infects the
red blood cells, which then accumulate in large amounts, blocking the
flow of blood in the capillaries of the brain and other organs.
The reason that the blood cells conglomerate and lodge in the blood
vessels is that once in the blood cell the parasite produces proteins
that project from the surface of the cell and bind with receptors on
other blood cells and on the vessel wall, and thus act like a glue. The
challenge facing scientists has been to break these bonds so that the
infected blood cells can be transported by the blood stream into the
spleen and destroyed.
The research group, which is headed by Professor Mats Wahlgren, has now
developed a substance that prevents infected blood cells from binding
in this way. The substance also releases blood cells already bound.
Using this method, scientists have been able to treat severe malaria in
rats and primates effectively; it now remains to be seen whether these
results can be replicated in people.
"There's often a lack of ability to treat people suffering from severe
malaria," says Professor Wahlgren. "We've developed a substance that
might be able to help these patients."
Previously, an anti-coagulant called heparin was used in the treatment
of severe malaria. Heparin was able to release the blood cells, but it
was soon withdrawn when it was shown that the substance caused internal
bleeding. The new substance is a development of heparin, and has the
important difference of having no effect on normal blood coagulation.
###
The study, which is jointly financed by Swedish International
Development Cooperation Agency and Dilafor AB, is to be presented on 29
September in PLoS Pathogens.
Publication:
"Release of sequestered malaria parasites upon injection of a
glycosaminoglycan," Anna M. Vogt, Fredrik Pettersson, Kirsten Moll,
Cathrine Jonsson, Johan Normark, Ulf Ribacke, Thomas G. Egwang,
Hans-Peter Ekre, Dorothe Spillmann, Qijun Chen and Mats Wahlgren, PLoS
Pathogens, September 2006, Vol. 2, Issue 9, e100.
For further information, please contact:
Professor Mats Wahlgren
Phone: +46-8-524 872 77, +46-70-556 12 46
Email: Mats.Wahlgren@ki.se
Postdoc Anna Vogt
Phonel: +46-8-457 25 09, +46-70-320 48 73
Email: Anna.Vogt@ki.se
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<<snip>>
these molecules may function as metal chelators
<<snip>>
Glycoconj J. 2003 Feb;20(2):133-41. Links
Glycosaminoglycans reduce oxidative damage induced by copper (Cu(+2)),
iron
(Fe(+2)) and hydrogen peroxide (H(2)O(2)) in human fibroblast cultures.
Campo GM, D'Ascola A, Avenoso A, Campo S, Ferlazzo AM, Micali C, Zanghi
L,
Calatroni A.
Department of Biochemical, Physiological and Nutritional Sciences,
School of
Medicine, university of Messina, Policlinico Universitario, 98125
Messina,
Italy. gca...@unime.it
Acid glycosaminoglycans (GAGs) antioxidant activity was assessed in a
fibroblast culture system by evaluating reduction of oxidative
system-induced
damage.Three different methods to induce oxidative stress in human skin
fibroblast cultures were used. In the first protocol cells were treated
with
CuSO(4) plus ascorbate. In the second experiment fibroblasts were
exposed to
FeSO(4) plus ascorbate. In the third system H(2)O(2) was utilised.The
exposition of fibroblasts to each one of the three oxidant systems
caused
inhibition of cell growth and cell death, increase of lipid
peroxidation
evaluated by the analysis of malondialdehyde (MDA), decrease of reduced
glutathione (GSH) and superoxide dismutase (SOD) levels, and rise of
lactate
dehydrogenase activity (LDH).The treatment with commercial GAGs at
different
doses showed beneficial effects in all oxidative models. Hyaluronic
acid (HA)
and chondroitin-4-sulphate (C4S) exhibited the highest protection.
However, the
cells exposed to CuSO(4) plus ascorbate and FeSO(4) plus ascorbate were
better
protected by GAGs compared to those exposed to H(2)O(2).These outcomes
confirm
the antioxidant properties of GAGs and further support the hypothesis
that
these molecules may function as metal chelators. Published in 2004.
PMID: 15001845 [PubMed - in process]
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