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Titolo:
THE MALARIA PARASITE SUPPLIES GLUTATHIONE TO ITS HOST-CELL - INVESTIGATION OF GLUTATHIONE TRANSPORT AND METABOLISM IN HUMAN ERYTHROCYTES INFECTED WITH PLASMODIUM-FALCIPARUM
Autore:
ATAMNA H; GINSBURG H;
Indirizzi:
HEBREW UNIV JERUSALEM,INST LIFE SCI,DEPT BIOL CHEM IL-91904 JERUSALEMISRAEL HEBREW UNIV JERUSALEM,INST LIFE SCI,DEPT BIOL CHEM IL-91904 JERUSALEMISRAEL
Titolo Testata:
European journal of biochemistry
fascicolo: 3, volume: 250, anno: 1997,
pagine: 670 - 679
SICI:
0014-2956(1997)250:3<670:TMPSGT>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
RED-BLOOD-CELLS; DEFICIENT HUMAN-ERYTHROCYTES; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; SUPEROXIDE-DISMUTASE; REDUCED GLUTATHIONE; REDUCTASE; DEFENSE; GLUCOSE-6-PHOSPHATE-DEHYDROGENASE; CATALASE;
Keywords:
PLASMODIUM FALCIPARUM; GLUTATHIONE; GAMMA-GLUTAMYLCYSTEINE; SYNTHESIS; OXIDATIVE STRESS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
65
Recensione:
Indirizzi per estratti:
Citazione:
H. Atamna e H. Ginsburg, "THE MALARIA PARASITE SUPPLIES GLUTATHIONE TO ITS HOST-CELL - INVESTIGATION OF GLUTATHIONE TRANSPORT AND METABOLISM IN HUMAN ERYTHROCYTES INFECTED WITH PLASMODIUM-FALCIPARUM", European journal of biochemistry, 250(3), 1997, pp. 670-679

Abstract

Malaria-infected red blood cells are under a substantial oxidative stress, Glutathione metabolism may play an important role in antioxidantdefense in these cells, as it does in other eukaryotes, In this work,we have determined the levels of reduced and oxidized glutathione (GSH and GSSG, respectively) and their distributions in the parasite, andin the host-cell compartments of human erythrocytes infected with themalaria parasite Plasmodium falciparum. In intact trophozoite-infected erythrocytes, [GSH] is low and [GSSG] is high, compared with the levels in normal erythrocytes, Normal erythrocytes and the parasite compartment display high GSH/GSSG ratios of 321.6 and 283.5, respectively, indicating adequate antioxidant defense. This ratio drops to 26.7 in the host-cell compartment, indicating a forceful oxidant challenge, thelow ratios resulting from an increase in GSSG and a decline in GSH concentrations. On the other hand, the concentrations of GSH and GSSG inthe parasite compartment remain physiological and comparable to theirconcentrations in normal red blood cells. This results from de novo glutathione synthesis and its recycling. assisted by the intensive activity of the hexose monophosphate shunt in the parasite. A large effluxof GSSG from infected cells has been observed, its rate being similarfi om free parasites and from intact infected cells. This result suggests that de novo synthesis by the parasite is the dominating process in infected cells. GSSG efflux from the intact infected cell is more than 60-fold higher than the rate observed in normal erythrocytes, and is mediated by permeability pathways that the parasite induces in the erythrocyte's membrane. The main route for GSSG efflux through the cytoplasmic membrane of the parasite seems to be due to a specific transport system and occurs against a concentration gradient. gamma-Glutamylcysteine [Glu(-Cys)] and GSH can penetrate through the pathways from the extracellular space into the host cytosol, but not into that of theparasite. This implies that the parasite membrane is impermeable to these peptides, and that the host cannot supply GSH to the parasite as suggested previously. Exogenous Glu(-Cys) is not converted into GSH inthe host cell, arguing that GSH synthetase may not be functional. Compartment analysis of Mg2+ in infected erythrocytes revealed that the host compartment exhibits a low concentration of Mg2+ (0.5 mM) in comparison with the parasite compart ment (4 mN) and the normal erythrocytes (1.5-3 mM). The drop in [Mg2+] results in cessation of Glu(-Cys) synthesist and hence or GSH synthesis in the host-cell compartment. The decrease in [Mg2+] can affect other Mg2+-ATP-dependent functions, such as Na+ and Ca2+ active efflux. The present investigation confirms thatthe host-cell compartment is oxidatively distressed, whereas the parasite is efficiently equipped with anti-oxidant means that protect the parasite from the oxidative injury. The parasite has a huge capacity for de novo synthesis of GSH and for the reduction of GSSG. Part of theGSSG that is actively extruded from the parasite is reduced to GSH inthe host cell whose own GSH synthesis is crippled.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 06:49:11