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Does myoglobin protect Trypanosoma cruzi from the antiparasitic effects of nitric oxide? 1
Author(s) -
Ascenzi Paolo,
Salvati Luca,
Brunori Maurizio
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02637-0
Subject(s) - trypanosoma cruzi , chagas disease , nitric oxide , myoglobin , antiparasitic agent , chemistry , intracellular , biochemistry , hemoglobin , nitrate reductase , ferric , antiparasitic , heme , microbiology and biotechnology , scavenger , ferrous , biology , parasite hosting , virology , antioxidant , pharmacology , enzyme , medicine , organic chemistry , world wide web , computer science , pathology
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.