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J Golenser, J Miller, DT Spira, T Navok and M Chevion
We examined the hypothesis that G-6-PD deficiency associated with fava bean
ingestion confers resistance to malaria by studying the in vitro
interactions between malaria parasites (Plasmodium falciparum), human
erythrocytes with varying degrees of G-6-PD deficiency, and isouramil (IU),
a fava bean extract that is known to cause oxidant stress and hemolysis of
G-6-PD-deficient erythrocytes. Untreated G-6-PD-deficient and normal
erythrocytes supported the in vitro growth of P. falciparum equally well.
However, after pretreatment with IU, G-6-PD-deficient erythrocytes did not
support parasite growth in vitro, whereas growth remained high in normal
erythrocytes. Parasite growth was proportional to the G-6-PD activity of
the IU-treated erythrocytes. In contrast, when parasitized erythrocytes
were exposed to IU, parasites even in normal erythrocytes were destroyed.
Ring forms were much less sensitive than late trophozoites and schizonts.
The results suggest that there are two modes by which IU affects the
development of P. falciparum and demonstrate in vitro that G-6-PD
deficiency confers resistance against malaria under conditions of
fava-bean-associated oxidant stress.
This article has been cited by other articles:
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| Copyright © 1983 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
