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Activity of divicine in Plasmodium vinckei ‐infected mice has implications for treatment of favism and epidemiology of G‐6‐PD deficiency
Author(s) -
Clark I. A.,
Cowden W. B.,
Hunt N. H.,
Maxwell L. E.,
Mackie E. J.
Publication year - 1984
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1984.tb02922.x
Subject(s) - haemolysis , glucose 6 phosphate dehydrogenase , glucose 6 phosphate dehydrogenase deficiency , hemolytic anemia , immunology , malaria , biology , glucosephosphate dehydrogenase deficiency , plasmodium falciparum , in vitro , microbiology and biotechnology , enzyme , biochemistry , dehydrogenase
S ummary. Intravenous injection of divicine into mice infected with Plasmodium vinckei rapidly killed the parasites and caused haemolysis. Degenerating parasites were observed frequently inside intact circulating erythrocytes, implying that parasite death was not a passive consequence of haemolysis. Both parasite death and haemolysis were prevented by the iron chelator desferrioxamine. In vitro , divicine caused the accumulation of malonyldialdehyde and the depletion of reduced glutathione in normal mouse erythrocytes. Desferrioxamine inhibited the former event, but not the latter. These observations support the hypothesis advanced by Huheey & Martin (Experientia , 31 , 1145, 1975) to explain the patchy geographical distribution of glucose‐6‐phosphate dehydrogenase deficiency in historic malarial areas and also suggest that desferrioxamine, a drug already in clinical use, is a potential treatment for favism and other examples of oxidative haemolysis.