Article Text

Hemoglobin Serves to Protect Plasmodium Parasites from Nitric Oxide and Reactive Oxygen Species
  1. Peter Sobolewski,
  2. Irene Gramaglia,
  3. John A. Frangos,
  4. Marcos Intaglietta,
  5. Henri C. van der Heyde
  1. From the La Jolla Bioengineering Institute (P.S., I.G., J.F., M.I., H.C.H.), La Jolla, CA. Supported by National Institutes of Health grants to J.F. (HL40696), M.I. (R24 HL643952), and H.C.H. (AI40667).
  1. Address correspondence to: Dr. Henri C. van der Heyde, La Jolla Bioengineering Institute, 505 Coast Boulevard South, La Jolla, CA 92037; tel: 858-456-7500; fax: 858-456-7540; e-mail: hvande{at}


ABSTRACT Our understanding of how the host immune response kills Plasmodium, the causative agent of malaria, is limited and controversial. One widely held belief is that reactive oxygen species are crucial for controlling parasite replication. One of the hallmarks of blood-stage malaria is the cyclic rupture of erythrocytes by the parasite, which releases free hemoglobin into the circulation. We propose that this free hemoglobin, as well as the hemoglobin within the erythrocyte and surrounding the parasite, effectively shields Plasmodium from reactive oxygen species well in excess of those achievable in vivo.

Key Words
  • nitric oxide
  • reactive oxygen species
  • malaria
  • Plasmodium
  • hemoglobin

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