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Verfasst von:Haag, Marvin [VerfasserIn]   i
 Kehrer, Jessica [VerfasserIn]   i
 Sanchez, Cecilia P. [VerfasserIn]   i
 Deponte, Marcel [VerfasserIn]   i
 Lanzer, Michael [VerfasserIn]   i
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

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