Plasmodium falciparum: Thiol status and growth in normal and glucose-6-phosphate dehydrogenase deficient human erythrocytes

Jacqueline Miller, Jacob Golenser, Dan T. Spira, Nechama S. Kosower

Research output: Contribution to journalArticlepeer-review

Abstract

The relationship of the thiol status of the human erythrocyte to the in vitro growth of Plasmodium falciparum in normal and in glucose-6-phosphate dehydrogenase (G6PD)-deficient red cells was investigated. Pretreatment with the thiol-oxidizing agent diamide led to inhibition of growth of P. falciparum in G6PD-deficient cells, but did not affect parasite growth in normal cells. Diamidetreated normal erythrocytes quickly regenerated intracellular glutathione (GSH) and regained normal membrane thiol status, whereas G6PD-deficient cells did not. Parasite invasion and intracellular development were affected under conditions in which intracellular GSH was oxidized to glutathione disulfide and membrane intrachain and interchain disulfides were produced. An altered thiol status in the G6PD-deficient erythrocytes could underlie the selective advantage of G6PD deficiency in the presence of malaria.

Original languageEnglish
Pages (from-to)239-247
Number of pages9
JournalExperimental Parasitology
Volume57
Issue number3
DOIs
StatePublished - Jun 1984

Keywords

  • Diamide
  • Erythrocyte
  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency
  • Malaria, human
  • Plasmodium falciparum
  • Protozoa, parasitic
  • Thiol status

Fingerprint

Dive into the research topics of 'Plasmodium falciparum: Thiol status and growth in normal and glucose-6-phosphate dehydrogenase deficient human erythrocytes'. Together they form a unique fingerprint.

Cite this