在一个人性化的小鼠模型中,primaquine-5,6-orthoquinone对老年G6PD缺陷红细胞有直接的血溶作用

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.).

概括

普里马奎因和塔费诺奎因用于治疗疟疾,但可能导致葡萄糖6酸脱酶缺乏症 (G6PDd) 患者的血液溶解. 这项研究表明,5,6-POQ,一种代谢物,直接导致G6PDd红细胞的血液溶解.