The enzymes of the glycolytic pathway in erythrocytes infected with Plasmodium falciparum malaria parasites

Abstract

Enzymes of the glycolytic pathway as well as some ancillary enzymes were studied in normal red cells parasitized with Plasmodium falciparum in culture at varying parasitemias as well as in isolated parasites. The levels of all enzymes except diphosphoglycerate mutase, glucose-6- phosphate dehydrogenase, and adenylate kinase were elevated. Extreme elevations of hexokinase, aldolase, enolase, pyruvate kinase, and adenosine deaminase concentrations were noted. In most cases, electrophoretically distinct bands of enzyme activity were also seen. These findings partly explain the previously noted 50- to 100-fold increase in glucose consumption of infected red cells and suggest that further knowledge of these parasite enzymes and their genetic basis may aid both in designing new chemotherapy and in understanding the evolution of these parasites.

Involvement of free radicals in parasitic infestations

“…Similar findings were reported in other parasitic infections. It has been reported that plasmodium-infected erythrocytes showed a decreased capacity of their antioxidant enzymes, including SOD (Friedman 1979;Wozencraft 1986;Erel et al 1997), CAT, GSH-PX (Greve et al 1999), G6PD (Roth et al 1988), methemoglobin reductase (Stocker et al 1985) and Vitamin E (Griffiths et al 2001).…”

Erythrocyte variants and the nature of their malaria protective effect

“…1), and as the parasite is heavily dependent on glycolysis, PK deficiency may partly impair parasite replication. Infection by Plasmodium has been shown to increase glucose consumption of red cells by 50-100 fold, as well as resulting in a substantial increase in glycolytic enzyme levels (Oelshlegel et al, 1975;Roth et al, 1988b). However, as the mature red cell is no longer capable of synthesizing enzymes and stimulation of existent enzymes seems unlikely, it was postulated that this increase was resulting from the parasite.…”

Immunization with PfEMP1-DBL1α generates antibodies that disrupt rosettes and protect against the sequestration of Plasmodium falciparum-infected erythrocytes

“…The protective effect afforded by deficiencies in pyruvate kinase, an enzyme involved in glycolyis for provision of energy to mature erythrocytes, is presently under investigation, although, studies in mouse models hint that this indeed might be the case (Roth et al, 1988;Min-Oo et al, 2003). Additionally, mutations in erythrocyte membrane proteins such as erythrocyte band 3 protein, ankyrin, spectrin and glycophorin C have also been shown to confer protection against malaria (Genton et al, 1995;Allen et al, 1999;Gallagher et al, 2004).…”