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

P Ascenzi1, L Salvati, M Brunori

  • 1Department of Biology, University Roma Tre, Rome, Italy. ascenzi@bio.uniroma3.it

FEBS Letters
|July 27, 2001
PubMed

Insights

Trypanosoma cruzi, the parasite causing Chagas disease, may survive in heart cells by using myoglobin (Mb) to neutralize harmful nitric oxide (NO). This novel function of Mb protects the parasite from NO’s lethal effects.

Area of Science:

  • Parasitology
  • Cardiology
  • Biochemistry

Background:

  • Chagas disease, caused by Trypanosoma cruzi, leads to fatal cardiomyopathy in South and Central America.
  • The parasite preferentially colonizes cardiomyocytes, the heart muscle cells.

Purpose of the Study:

  • To investigate the potential role of myoglobin (Mb) in protecting Trypanosoma cruzi within cardiomyocytes.
  • To explore a novel function of Mb as a nitric oxide (NO) scavenger against parasite-toxic NO levels.

Main Methods:

  • The study is based on existing biochemical knowledge of Mb-NO interactions.
  • It postulates a mechanism involving ferrous oxygenated Mb reacting with NO to form nitrate.
  • It suggests an intracellular reductase regenerates active Mb.

Main Results:

  • Ferrous oxygenated Mb rapidly and irreversibly reacts with NO, producing nitrate.
  • This reaction yields ferric oxidized Mb, which can be reduced back to its active form.

Conclusions:

  • Myoglobin may protect Trypanosoma cruzi from the lethal effects of nitric oxide in cardiomyocytes.
  • This proposed Mb function is analogous to hemoglobin's protective role for Plasmodia in red blood cells.

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