Does myoglobin protect Trypanosoma cruzi from the antiparasitic effects of nitric oxide?

P. Ascenzi, L. Salvati, M. Brunori

Research output: Contribution to journalArticlepeer-review

Abstract

The hemoflagellate protozoan parasite Trypanosoma cruzi is the causative agent of Chagas disease, a progressive fatal cardiomyopathy widespread in South and Central America. Here, we postulate that the preferential colonization of cardiomyocytes by T. cruzi may reflect the role of myoglobin (Mb) as a nitric oxide (NO) scavenger, protecting the parasite from the trypanocidal effects of NO. The proposal of this novel function of Mb is based on knowledge that ferrous oxygenated Mb reacts rapidly and irreversibly with NO yielding nitrate and ferric oxidized Mb, which is reduced back to the physiologically active form by an intracellular reductase. The postulated protective role of Mb on the viability of T. cruzi is reminiscent of that postulated for hemoglobin in protecting intraerythrocytic Plasmodia from the parasiticidal effect of NO.

Original languageEnglish
Pages (from-to)103-105
Number of pages3
JournalFEBS Letters
Volume501
Issue number1-3
Publication statusPublished - Jul 20 2001

Keywords

  • Myoglobin
  • Nitric oxide
  • Trypanosoma cruzi

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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