Iron deficiency influences the course of malaria in Plasmodium berghei infected mice

Biochem Biophys Res Commun. 2007 Jun 8;357(3):608-14. doi: 10.1016/j.bbrc.2007.03.175. Epub 2007 Apr 9.


Iron deficiency accelerates suicidal erythrocyte death, which is evident from phosphatidylserine exposure. The present study explored whether iron deficiency compromises intraerythrocytic growth of Plasmodium and enhances death of infected erythrocytes thus influencing the course of malaria. As a result, phosphatidylserine exposure is increased in Plasmodium falciparum infected human erythrocytes, an effect significantly more marked in iron deficiency. Moreover, iron deficiency impairs in vitro intraerythrocytic growth and infection of erythrocytes. In mice, iron-deficient erythrocytes are more rapidly cleared from circulating blood, an effect increased by infection with Plasmodium berghei. Parasitemia in P. berghei infected mice was significantly decreased (from 54% to 33% of circulating erythrocytes 20 days after infection) and mouse survival significantly enhanced (from 0% to 20% 30 days after infection) in iron-deficient mice. In conclusion, iron deficiency favourably influences the course of malaria, an effect partially due to accelerated suicidal death and subsequent clearance of infected erythrocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Erythrocytes / drug effects
  • Erythrocytes / metabolism*
  • Erythrocytes / parasitology
  • Female
  • Flow Cytometry / methods
  • Humans
  • Iron Deficiencies*
  • Malaria / blood
  • Malaria / metabolism*
  • Malaria / parasitology
  • Mice
  • Mice, Inbred C57BL
  • Phosphatidylserines / pharmacology
  • Plasmodium berghei / growth & development*
  • Plasmodium falciparum / drug effects
  • Plasmodium falciparum / growth & development


  • Phosphatidylserines