Physiological jump in erythrocyte redox potential during Plasmodium falciparum development occurs independent of the sickle cell trait
The redox state of the host-parasite unit has been hypothesized to play a central role for the fitness of the intraerythrocytic blood stages of the human malaria parasite Plasmodium falciparum. In particular, hemoglobinopathies have been suggested to cause a more oxidizing environment, thereby prote...
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| Main Authors: | , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
16 November 2022
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| In: |
Redox Biology
Year: 2022, Volume: 58, Pages: 1-13 |
| ISSN: | 2213-2317 |
| DOI: | 10.1016/j.redox.2022.102536 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.redox.2022.102536 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S2213231722003081 
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| Author Notes: | Marvin Haag, Jessica Kehrer, Cecilia P. Sanchez, Marcel Deponte, Michael Lanzer |
MARC
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| 520 | |a The redox state of the host-parasite unit has been hypothesized to play a central role for the fitness of the intraerythrocytic blood stages of the human malaria parasite Plasmodium falciparum. In particular, hemoglobinopathies have been suggested to cause a more oxidizing environment, thereby protecting from severe malaria. Here we determined the redox potential of infected wild-type (hemoglobin AA) or sickle trait (hemoglobin AS) erythrocytes using parasite-encoded variants of the redox-sensitive green-fluorescent protein 2 (roGFP2). Our non-invasive roGFP2 single-cell measurements revealed a reducing steady-state redox potential of −304 ± 11 mV for the erythrocyte cytosol during ring-stage development and a rather sudden oxidation to −278 ± 12 mV during trophozoite-stage development around 28 h post invasion. There was no significant difference between wild-type or sickle trait erythrocytes regarding the stage dependence and the detected increase of the redox potential during the intraerythrocytic life cycle. The steady-state redox potential of the parasite cytosol, between −304 and −313 mV, was highly reducing throughout the life cycle. The redox potential in the parasitophorous vacuole at the interface between the secretory pathway and the erythrocyte was −284 ± 10 mV and remained stable during trophozoite-stage development with implications for the export of disulfide-containing proteins. In summary, P. falciparum blood stage development from the late ring to the early trophozoite stage causes a physiological jump in erythrocyte redox potential irrespective of the presence or absence of hemoglobin S. | ||
| 650 | 4 | |a Erythrocyte redox potential | |
| 650 | 4 | |a Genetically encoded redox sensors | |
| 650 | 4 | |a Glutathione | |
| 650 | 4 | |a Oxidation | |
| 650 | 4 | |a Plasmodium falciparum infected red blood cells | |
| 650 | 4 | |a Reduction | |
| 650 | 4 | |a roGFP2 | |
| 650 | 4 | |a Secretory pathway | |
| 650 | 4 | |a Sickle cell trait | |
| 700 | 1 | |a Kehrer, Jessica |d 1981- |e VerfasserIn |0 (DE-588)1158624816 |0 (DE-627)102060610X |0 (DE-576)504253263 |4 aut | |
| 700 | 1 | |a Sanchez, Cecilia P. |e VerfasserIn |0 (DE-588)1079241388 |0 (DE-627)840669348 |0 (DE-576)452286093 |4 aut | |
| 700 | 1 | |a Deponte, Marcel |e VerfasserIn |4 aut | |
| 700 | 1 | |a Lanzer, Michael |e VerfasserIn |0 (DE-588)1065643314 |0 (DE-627)816506736 |0 (DE-576)165563826 |4 aut | |
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