Lipid peroxidation in Plasmodium falciparum-parasitized human erythrocytes

• Published in: Archives of biochemistry and biophysics Vol. 298; no. 2; pp. 651 - 657
• Main Authors: Simões, Ana Paula C.F., van den Berg, Jeroen J.M., Roelofsen, Ben, Op den Kamp, Jos A.F.
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 01.11.1992; Elsevier
• Subjects: Animals; Ascorbic Acid - pharmacology; Benzene Derivatives - pharmacology; Biological and medical sciences; Cytosol - metabolism; Erythrocyte Membrane - metabolism; Erythrocytes - drug effects; Erythrocytes - metabolism; Erythrocytes - parasitology; Experimental protozoal diseases and models; Fatty Acids, Unsaturated - blood; Humans; In Vitro Techniques; Infectious diseases; Lipid Peroxidation; Medical sciences; Oxidation-Reduction; Parasitic diseases; Plasmodium falciparum; Plasmodium falciparum - pathogenicity; Protozoal diseases; Vitamin E - blood; Human; Protozoa; Plasmodium falciparum; Sensitivity resistance; Plasma membrane; Red blood cell; Lipids; Host agent relation; Sporozoa; In vitro; Peroxidation
• ISSN: 0003-9861; 1096-0384
• DOI: 10.1016/0003-9861(92)90462-6

cis-Parinaric acid (PnA) was used as a fluorescent probe to study lipid peroxidation in nonparasitized and Plasmodium falciparum-parasitized erythrocytes, upon challenge by cumene hydroperoxide and tert-butyl hydroperoxide. Parasitized erythrocytes were less susceptible toward lipid peroxidation than nonparasitized erythrocytes with which they had been cultured. Furthermore, nonparasitized erythrocytes cultured together with parasitized cells, and thereafter isolated on a Percoll gradient, were less susceptible toward lipid peroxidation than erythrocytes kept under the same experimental conditions but in the absence of parasitized cells. We concluded, therefore, that the intracellular development of the parasite leads to an increase in the resistance against oxidative stress, not only of the host cell membrane of the parasitized erythrocyte, but also in the plasma membrane of the neighboring cells. The erythrocyte cytosol of parasitized cells and/or the intraerythrocytic parasite was required for the increased protection of the host cell membrane, since ghosts prepared from parasitized erythrocytes were more susceptible to lipid peroxidation than those prepared from nonparasitized ones. Vitamin E content of parasitized erythrocytes was lower than that of nonparasitized cells. However, parasitized erythrocytes promoted extracellular reduction of ferricyanide at higher rates, which might be indicative of a larger cytosolic reductive capacity. It is suggested that the improved response of intact erythrocytes is due to an increased reduction potential of the host-erythrocyte cytosol. The role of vitamin C as a mediator of this process is discussed.