Summary
The extent of reduced glutathione, activity of glutathione peroxidase, amount of membrane lipid peroxidation products, and the extent of hemoglobin release from host erythrocytes during in vitroPlasmodium falciparum growth was studied. Highly synchronized parasite cultures were studied to examine the alterations caused by different growth stages of the parasite. There was a moderate increase in the reduced glutathione content as the parasite matured, which was significant only in schizontrich erythrocyte lysates (p<0.05) whereas the activity of glutathione peroxidase was significantly low in all the parasitized red blood cells (ring-infected RBC,p<0.005; trophozoite- and schizont-infected RBC,p<0.001). The lipid peroxidation product, malonyldialdehyde, of the host red cells increased gradually to more than fourfold in schizont-rich cells as compared with normal erythrocytes (p<0.001). The hemoglobin release from cultured cells was significantly higher in all parasitized red cell cultures as well as in uninfected cells kept in in vitro, as compared with normal erythrocytes. The consequence of such changes induced by the malarial parasites in the host red cells in the pathogenesis of erythrocyte destruction and anemia ofP. falciparum malaria is discussed.
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References
Arese P, Turrini F, Ginsburg H (1991) Erythrophagocytosis in malaria: host defence or menace to the macrophage. Parasitol Today 7: 25–28
Friedman MJ (1979) Oxidant damage mediates variant red cell resistance to malaria. Nature 280: 245–247
Golenser J, Marva E, Chevion M (1991) The survival of plasmodium under oxidant stress. Parasitol Today 7: 142–146
Hebbel RP, Shalev O, Foker W, Rank BH (1986) Inhibition of erythrocyte Ca2+ ATPase by activated oxygen through thiol and lipid-dependent mechanism. Biochem Biophys Acta 862: 8–16
Kaplan JM, Weidanz WP (1989) In: Stevenson MM (ed) Role of cell mediated immunity in resistance to malaria: host response to infection. CRC Press, Boca Raton, FL, pp 37–63
Lawrence RA, Burk RF (1976) Glutathione peroxidase activity in selinium-deficient rat liver. Biochem Biophys Res Commun 71: 952–957
Maguire PA, Sherman IW (1990) Phospholipid composition, cholesterol content and cholesterol exchange inPlasmodium falciparum-infected red cells. Mol Biochem Parasitol 38: 105–112
Maridonneau I, Braquet P, Garay RP (1983) Na+ and K+ transport damage induced by oxygen free radicals in human red cell membranes. J Biol Chem 256: 3107–3113
Mohan K, Dubey ML, Ganguly NK, Mahajan RC (1992)Plasmodium falciparum induced perturbations of the erythrocyte antioxidant system. Clin Chem Acta (in press)
Murray MC, Perkins ME (1989) Phosphorylation of erythrocyte membrane and cytoskeletal proteins in cells infected withPlasmodium falciparum. Mol Biochem Parasitol 34: 229–236
Rivadeneira EM, Wasserman M, Espinal CT (1983) Separation and concentration of schizonts ofPlasmodium falciparum by Percoll gradients. J Protozool 30: 367–370
Saltman P (1989) Oxidative stress: a radical view. Semin Haematol 26: 249–256
Sherman IW (1988) Mechanisms of molecular trafficking in malaria. Parasitol 96 [Suppl]: 57–81
Stocker R, Hunt NH, Buffinton GD, Weidemann MJ, Hughes PHL, Clark IA (1985) Oxidative stress and protective mechanisms in erythrocytes in relation toPlasmodium vinckei load. Proc Natl Acad Sci USA 82: 548–551
Trager W, Jensen JB (1976) Human malaria parasites in continuous culture. Science 193: 673–675
Weatherall DJ, Abdalla S, Pippard MJ (1983) Malaria and the red cell. Ciba Foundation symposium-94. Pitman, London, pp 74–97
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Mohan, K., Ganguly, N.K., Dubey, M.L. et al. Oxidative damage of erythrocytes infected with Plasmodium falciparum. Ann Hematol 65, 131–134 (1992). https://doi.org/10.1007/BF01695812
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DOI: https://doi.org/10.1007/BF01695812