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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
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.
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.