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Primaquine-5,6-Orthoquinone Is Directly Hemolytic to Older G6PD Deficient RBCs in a Humanized Mouse Model.

Karolina H Dziewulska-Cronk1, Julie A Reisz1, Ariel M Hay1

  • 1Department of Pathology, University of Virginia School of Medicine, Charlottesville, Virginia (K.H.D.-C., A.M.H., J.C.Z.); Carter Immunology Center, University of Virginia, Charlottesville, Virginia (K.H.D.-C., A.M.H., J.C.Z.); Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, Colorado (J.A.R., T.N., F.I.C., A.I., A.D-A.); University of Maryland, School of Medicine, Center for Blood Oxygen Transport and Hemostasis, Department of Pediatrics, Baltimore, Maryland (D.R.L., P.W.B.); Center for Biomedical Engineering and Technology, and Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland (E.A.L., J.P.Y.K.); University of Maryland School of Medicine, Department of Pathology, Baltimore, Maryland (M.S.P., P.W.B.); National Center for Natural Products Research, School of Pharmacy, University of Mississippi, University, Mississippi (L.A.W.); and GlobaCure, Birmingham, Alabama (B.L.T.).

The Journal of Pharmacology and Experimental Therapeutics
|August 2, 2024
PubMed
Summary

Primaquine and tafenoquine are used to treat malaria but can cause hemolysis in patients with glucose 6-phosphate dehydrogenase deficiency (G6PDd). This study shows that 5,6-POQ, a metabolite, directly causes hemolysis in G6PDd red blood cells.

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Area of Science:

  • Biochemistry
  • Hematology
  • Pharmacology

Background:

  • Primaquine and tafenoquine are crucial for radical cure of Plasmodium vivax malaria.
  • These drugs are contraindicated in glucose 6-phosphate dehydrogenase deficient (G6PDd) individuals due to hemolysis risk.
  • 5-hydroxyprimaquine and its metabolites are implicated in drug-induced hemolysis, but the role of 5,6-POQ is debated.

Purpose of the Study:

  • To investigate the hemolytic activity of 5,6-POQ, a metabolite of primaquine.
  • To establish a humanized mouse model for studying G6PD deficiency and drug-induced hemolysis.
  • To determine if 5,6-POQ directly contributes to hemolysis in G6PDd red blood cells.

Main Methods:

  • Developed a novel humanized mouse model with G6PD Mediterranean variant (hG6PDMed-) and a control (hG6PDND).
  • Performed in vitro challenge of red blood cells (RBCs) with 5,6-POQ to assess oxidative stress markers.
  • Administered 5,6-POQ to mice and analyzed in vivo clearance of RBCs based on age and G6PD status.

Main Results:

  • In vitro exposure to 5,6-POQ increased superoxide and methemoglobin generation in RBCs.
  • In vivo studies demonstrated selective clearance of older hG6PDMed- RBCs after 5,6-POQ infusion.
  • Established a functional humanized mouse model for G6PD deficiency, recapitulating age-dependent enzyme decay.

Conclusions:

  • 5,6-POQ directly induces reactive oxygen species (ROS) and hemolysis, particularly in older G6PDd RBCs.
  • Challenges the view of 5,6-POQ as an inert metabolite, suggesting it is a major hemolytic toxin.
  • Provides the first direct evidence that young G6PDd RBCs are resistant to primaquine-induced hemolysis.