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Beneficial effect of aurothiomalate on murine malaria.

Alesutan I, Bobbala D, Qadri SM, Estremera A, Föller M, Lang F - Malar. J. (2010)

Bottom Line: Exposure to aurothiomalate significantly decreased the in vitro parasitemia of P. falciparum-infected human erythrocytes without influencing the intraerythrocytic DNA/RNA content.All nontreated mice died within 30 days of infection.Sodium aurothiomalate influences the survival of Plasmodium berghei-infected mice, an effect only partially explained by stimulation of eryptosis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology, University of Tübingen, Gmelinstr, 5, 72076 Tübingen, Germany.

ABSTRACT

Background: Premature death of Plasmodium-infected erythrocytes is considered to favourably influence the clinical course of malaria. Aurothiomalate has previously been shown to trigger erythrocyte death or eryptosis, which is characterized by cell membrane scrambling leading to phosphatidylserine exposure at the cell surface. Phosphatidylserine-exposing cells are rapidly cleared from circulating blood. The present study thus tested whether sodium aurothiomalate influences the intraerythrocytic parasite development in vitro and the clinical course of murine malaria in vivo.

Methods: Human erythrocytes were infected with Plasmodium falciparum BinH in vitro and mice were infected (intraperitoneal injection of 1 x 106 parasitized murine erythrocytes) with Plasmodium berghei ANKA in vivo.

Results: Exposure to aurothiomalate significantly decreased the in vitro parasitemia of P. falciparum-infected human erythrocytes without influencing the intraerythrocytic DNA/RNA content. Administration of sodium aurothiomalate in vivo (daily 10 mg/kg b.w. s.c. from the 8th day of infection) enhanced the percentage of phosphatidylserine-exposing infected and noninfected erythrocytes in blood. All nontreated mice died within 30 days of infection. Aurothiomalate-treatment delayed the lethal course of malaria leading to survival of more than 50% of the mice 30 days after infection.

Conclusions: Sodium aurothiomalate influences the survival of Plasmodium berghei-infected mice, an effect only partially explained by stimulation of eryptosis.

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Effect of sodium aurothiomalate treatment on the hematocrit of Plasmodium berghei-infected mice. Arithmetic means ± SEM of packed cell volume (hematocrit) in mice without treatment (open circles, n = 8 mice) or with daily 10 mg/kg b.w. s.c. of sodium aurothiomalate (closed circles, n = 8 mice) as a function of days after infection with P. berghei. * indicates significant difference (p < 0.05; t-test).
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Figure 5: Effect of sodium aurothiomalate treatment on the hematocrit of Plasmodium berghei-infected mice. Arithmetic means ± SEM of packed cell volume (hematocrit) in mice without treatment (open circles, n = 8 mice) or with daily 10 mg/kg b.w. s.c. of sodium aurothiomalate (closed circles, n = 8 mice) as a function of days after infection with P. berghei. * indicates significant difference (p < 0.05; t-test).

Mentions: Malaria is paralleled by loss of erythrocytes leading to anemia. As shown in Fig. 5, the hematocrit of aurothiomalate-treated mice was significantly reduced. The effect could have been due to enhanced eryptosis or hemolysis. In noninfected erythrocytes aurothiomalate has previously been shown to trigger eryptosis rather than hemolysis [44].


Beneficial effect of aurothiomalate on murine malaria.

Alesutan I, Bobbala D, Qadri SM, Estremera A, Föller M, Lang F - Malar. J. (2010)

Effect of sodium aurothiomalate treatment on the hematocrit of Plasmodium berghei-infected mice. Arithmetic means ± SEM of packed cell volume (hematocrit) in mice without treatment (open circles, n = 8 mice) or with daily 10 mg/kg b.w. s.c. of sodium aurothiomalate (closed circles, n = 8 mice) as a function of days after infection with P. berghei. * indicates significant difference (p < 0.05; t-test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2875225&req=5

Figure 5: Effect of sodium aurothiomalate treatment on the hematocrit of Plasmodium berghei-infected mice. Arithmetic means ± SEM of packed cell volume (hematocrit) in mice without treatment (open circles, n = 8 mice) or with daily 10 mg/kg b.w. s.c. of sodium aurothiomalate (closed circles, n = 8 mice) as a function of days after infection with P. berghei. * indicates significant difference (p < 0.05; t-test).
Mentions: Malaria is paralleled by loss of erythrocytes leading to anemia. As shown in Fig. 5, the hematocrit of aurothiomalate-treated mice was significantly reduced. The effect could have been due to enhanced eryptosis or hemolysis. In noninfected erythrocytes aurothiomalate has previously been shown to trigger eryptosis rather than hemolysis [44].

Bottom Line: Exposure to aurothiomalate significantly decreased the in vitro parasitemia of P. falciparum-infected human erythrocytes without influencing the intraerythrocytic DNA/RNA content.All nontreated mice died within 30 days of infection.Sodium aurothiomalate influences the survival of Plasmodium berghei-infected mice, an effect only partially explained by stimulation of eryptosis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology, University of Tübingen, Gmelinstr, 5, 72076 Tübingen, Germany.

ABSTRACT

Background: Premature death of Plasmodium-infected erythrocytes is considered to favourably influence the clinical course of malaria. Aurothiomalate has previously been shown to trigger erythrocyte death or eryptosis, which is characterized by cell membrane scrambling leading to phosphatidylserine exposure at the cell surface. Phosphatidylserine-exposing cells are rapidly cleared from circulating blood. The present study thus tested whether sodium aurothiomalate influences the intraerythrocytic parasite development in vitro and the clinical course of murine malaria in vivo.

Methods: Human erythrocytes were infected with Plasmodium falciparum BinH in vitro and mice were infected (intraperitoneal injection of 1 x 106 parasitized murine erythrocytes) with Plasmodium berghei ANKA in vivo.

Results: Exposure to aurothiomalate significantly decreased the in vitro parasitemia of P. falciparum-infected human erythrocytes without influencing the intraerythrocytic DNA/RNA content. Administration of sodium aurothiomalate in vivo (daily 10 mg/kg b.w. s.c. from the 8th day of infection) enhanced the percentage of phosphatidylserine-exposing infected and noninfected erythrocytes in blood. All nontreated mice died within 30 days of infection. Aurothiomalate-treatment delayed the lethal course of malaria leading to survival of more than 50% of the mice 30 days after infection.

Conclusions: Sodium aurothiomalate influences the survival of Plasmodium berghei-infected mice, an effect only partially explained by stimulation of eryptosis.

Show MeSH
Related in: MedlinePlus