Redox metabolism in glucose-6-phosphate dehydrogenase deficient erythrocytes and its relation to antimalarial chemotherapy.
Experiments in glucose-6-phosphate dehydrogenase (G6PD) deficient erythrocytes parasitized by Plasmodium falciparum proved that depletion of glutathione increased fluxes of reactive oxygen species and was detrimental to the parasite at various sites and developmental stages. Chloroquine is also considered an inducer of oxidant damage due to its role in preventing heme polymerization. Recently it has been found that GSH prevents cellular damage by degrading the toxic heme. Consequently, we suggest that the use of combinations of chloroquine and depletors of GSH would be highly efficient for the chemotherapy of malaria.
Ginsburg
H
H
Department of Biological Chemistry, Hebrew University of Jerusalem, Israel.
Golenser
J
J
D000818:Animals; D000962:Antimalarials / Q000627:therapeutic use*; D002478:Cells, Cultured; D002738:Chloroquine / Q000627:therapeutic use; D004912:Erythrocytes / Q000201:enzymology / Q000378:metabolism*; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000097:blood*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D017665:Hydroxyl Radical / Q000378:metabolism; D016778:Malaria, Falciparum / Q000188:drug therapy*; D010084:Oxidation-Reduction; D010963:Plasmodium falciparum / Q000187:drug effects
D000962:Antimalarials; D017665:Hydroxyl Radical; D002738:Chloroquine; D005978:Glutathione