Online-Ressource | |
Verfasst von: | Haag, Marvin [VerfasserIn] |
Kehrer, Jessica [VerfasserIn] | |
Sanchez, Cecilia P. [VerfasserIn] | |
Deponte, Marcel [VerfasserIn] | |
Lanzer, Michael [VerfasserIn] | |
Titel: | Physiological jump in erythrocyte redox potential during Plasmodium falciparum development occurs independent of the sickle cell trait |
Verf.angabe: | Marvin Haag, Jessica Kehrer, Cecilia P. Sanchez, Marcel Deponte, Michael Lanzer |
E-Jahr: | 2022 |
Jahr: | 16 November 2022 |
Umfang: | 13 S. |
Fussnoten: | Online verfügbar 10 November 2022, Artikelversion 16 November 2022 ; Gesehen am 25.01.2023 |
Titel Quelle: | Enthalten in: Redox Biology |
Ort Quelle: | Amsterdam [u.a.] : Elsevier, 2013 |
Jahr Quelle: | 2022 |
Band/Heft Quelle: | 58(2022) vom: Nov., Artikel-ID 102536, Seite 1-13 |
ISSN Quelle: | 2213-2317 |
Abstract: | 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. |
DOI: | doi:10.1016/j.redox.2022.102536 |
URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt. Volltext: https://doi.org/10.1016/j.redox.2022.102536 |
Volltext: https://www.sciencedirect.com/science/article/pii/S2213231722003081 | |
DOI: https://doi.org/10.1016/j.redox.2022.102536 | |
Datenträger: | Online-Ressource |
Sprache: | eng |
Sach-SW: | Erythrocyte redox potential |
Genetically encoded redox sensors | |
Glutathione | |
Oxidation | |
Plasmodium falciparum infected red blood cells | |
Reduction | |
roGFP2 | |
Secretory pathway | |
Sickle cell trait | |
K10plus-PPN: | 1832389111 |
Verknüpfungen: | → Zeitschrift |