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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cultured Plasmodium falciparum was retarded in intraerythrocytic development by serum from malaria-immune adults, by human TB serum, and by rabbit tumor necrosis serum. Neither the potency nor efficacy of any of these sera was altered by a variety of antioxidants or oxygen-free radial scavengers, including ascorbate, alpha-tocopherol, BHT, cystine or cysteine, glutathione, histidine, phenylalanine, tryptophan, tyrosine, superoxide dismutase, catalase (or combination of the two enzymes), or by reducing the ambient O2 tension to 1%. It is thus unlikely that the antiparasitic activity of these inhibitory sera can be attributed to oxidative mechanisms.
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PMID:Antioxidants do not prevent the in vitro induction of Plasmodium falciparum crisis forms by human malaria-immune, TB or rabbit TNF serum. 352 84

Hydrogen peroxide (H2O2) has been incriminated to have an oxidative killing malaria parasite. As P. berghei-infected mouse red cells generated H2O2 in vivo, this would result in the alteration of catalase status of the host. The present study was undertaken to determine catalase activity in red cells and liver of mice infected with P. berghei. The studies were performed in 17 samples of infected red cells as well as 20 samples of the normal red cells. Results showed that the catalase activity in red cells of the infected group was significantly lower (p less than 0.01) than that of the normal group. There was a reverse relationship between catalase activity and parasitemia. Crude parasite lysates possessed no catalase activity. Liver catalase content in the infected group was also found to be significantly lower (p less than 0.05) than that of the control group. All these findings indicated that P. berghei-infected mice caused a depressed catalase activity in red cells and liver which was possibly due to the catalatic function in detoxifying the increased H2O2 to water and free oxygen.
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PMID:Catalase activity in red cell and liver of mice infected with Plasmodium berghei. 352 80

Plasmodium berghei, a murine malaria, lacks endogenous superoxide dismutase (SOD). Instead it appears to take up and concentrate SOD from its host cell, the erythrocyte. We now demonstrate that the adopted host enzyme is localized in granules which are probably lysosomes. In addition, isolated P. berghei parasites contain only low levels of catalase, probably as a result of contamination of the preparation with host cell material. Thus, the cytosol of this organism appears to be deficient in enzymes which protect against damage by activated oxygen.
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PMID:Superoxide dismutase and catalase in the murine malaria, Plasmodium berghei: content and subcellular distribution. 353 81

The in vitro growth of Plasmodium falciparum in red cells containing haemoglobin E (HbE) was studied at oxygen concentration of 5 to 20%, with and without antioxidants. Under all conditions, parasite growth decreased as the concentration of HbE increased as compared with growth in red cells containing only HbA. The decreases were proportionately greatest at the highest oxygen concentration. The antioxidant vitamin C partially reversed the decreases in growth observed in HbE-containing cells at 20% oxygen. South-east Asian refugees with HbAE or HbEE had high antimalarial IFA titres, indicative of exposure to malaria more frequently than did refugees with HbAA. The decreased growth of P. falciparum in HbE-containing red cells may reduce the severity of malaria infections, conferring a survival advantage and thus increasing the numbers of individuals with HbE in local areas of South-east Asia with high incidences of malaria.
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PMID:Decreased growth of Plasmodium falciparum in red cells containing haemoglobin E, a role for oxidative stress, and a sero-epidemiological correlation. 354 62

Experiments with malaria in mice suggest that protective immunity depends not only on antibody but also on activation of macrophages. Activated macrophages may cause intra-erythrocytic death of parasites by releasing reactive oxygen intermediates and/or tumour necrosis factor. Macrophage activation for both types of product correlates well with the timing of recovery in a range of different malaria infections and in mice protected by vaccination.
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PMID:Macrophages as effector cells in immunity to malaria. 391 May 70

Ten cases of pulmonary involvement associated with falciparum malaria are described. Measurements of pulmonary capillary wedge pressure were made in five of the ten cases, and no evidence of raised hydrostatic pressure in the pulmonary microcirculation was found which could account for the pulmonary oedema observed. All cases were treated with oxygen and positive end expiratory pressure (PEEP), and there were six survivors. The evidence to support the presence of an Adult Respiratory Distress Syndrome (ARDS)-type lesion in malaria is discussed.
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PMID:Pulmonary damage associated with falciparum malaria: a report of ten cases. 391 86

Swiss mice with chronic Trypanosoma brucei infections become refractory to subsequent infection with Babesia microti and B. rodhaini. Infection with B. microti 7 days after T. brucei resulted in an obvious inhibition of the babesia parasitaemias and this inhibition became more profound as the time interval between the infections increased, until at 17-20 days the parasitaemias were totally abolished. Even after intravenous injection of large numbers of parasites parasitaemias were inhibited. Similar inhibition was obtained in BALB/c mice but not in C57BL/6 mice. Mice with established T. brucei infections also showed reduced susceptibility to B. rodhaini. In mice similarly infected with T. brucei and the malaria parasites Plasmodium chabaudi chabaudi and P. c. adami the pre-patent periods were noticeably prolonged but the subsequent parasitaemias were unaffected. Infections with P. yoelii were unaffected. Trypanosoma brucei infections were not affected by the intracellular parasites. Among the mechanisms investigated to explain these findings were changes in red blood cell populations, cross-reacting antigens, the release of toxic factors and the generation of activated oxygen species. None of these could account for the inhibition observed.
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PMID:Interactions between Trypanosoma brucei and Babesia spp. and Plasmodium spp. in mice. 400 Jul 2

Asexual blood forms of malaria parasites are microaerophilic and sensitive to oxidant stress. Plasmodium falciparum and some other species of malaria parasites undergo schizogony attached to endothelial cells of postcapillary venules, where oxygen tensions are low. Acquired immune responses to all forms of malaria parasites so far investigated are thymus dependent. Animals deprived of T lymphocytes do not recover from the infections and cannot be immunized against malaria parasites. In contrast, animals unable to make antibodies recover normally from some primary infections, e.g. with Plasmodium chabaudi, and when rescued by chemotherapy from other species of malaria parasite develop lasting, nonsterile immunity. Immunity to malaria can be transferred in mice by T lymphocytes of the Ly1+ phenotype, but transfer of B lymphocytes together with this T-cell subset increases the effectiveness of immunity to Plasmodium yoelii. Thus, antibodies facilitate recovery from some primary malaria infections and increase the effectiveness of cell-mediated immune responses in these infections. Mice of the A strain are highly susceptible to malaria and are unable to increase the number of mononuclear cells in the spleen during the course of the infections. It is postulated that T lymphocytes responding to parasite antigens release factors that stimulate the proliferation of effector cell precursors and their recruitment into the red pulp of the spleen. In this site, the liver and probably the peripheral circulation, effector cells bind to the surface of parasitized erythrocytes and are activated to release superoxide (O2-). The consequent exposure to oxidant stress can lead to degeneration of parasites in erythrocytes. This effect on the parasites can be prevented by agents chelating metals, which suggests that iron-catalyzed lipid peroxidation and consequent K+ loss, or inactivation of metal-containing enzymes, may be the mechanism by which oxidant stress kills the intracellular parasites. Antibodies on the surface of schizont-infected cells could facilitate binding of effector cells and trigger O2- release, thereby acting synergistically with cell-mediated immunity. Inherited traits, such as abnormal hemoglobins and G-6-PD deficiency, and acquired cell-mediated immunity both subject malaria parasites to oxidant stress and may reinforce one another, increasing the chances of survival of children bearing these traits during the dangerous years of first exposure to malaria in areas where the disease is endemic.
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PMID:The role of cell-mediated immune responses in resistance to malaria, with special reference to oxidant stress. 610 May 38

Aerobic organisms depend on superoxide dismutase to suppress the formation of dangerous species of activated oxygen. Intraerythrocytic stages of the malaria parasite exist within a highly aerobic environment and cause the generation of increased amounts of activated oxygen. Plasmodium berghei in mice was found to derive a substantial amount of superoxide dismutase activity from the host cell cytoplasm. Plasmodia isolated from mouse red cells contained mouse superoxide dismutase, whereas rat-derived parasites contained the rat enzyme. This is believed to be the first example of the acquisition of a host cell enzyme by an intracellular parasite.
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PMID:Malaria parasites adopt host cell superoxide dismutase. 634 44

Antimalarial effects might be expected from compounds that modify hemoglobin. Dibromoaspirin and bis(dibromosalicyl) diesters decrease gelation of hemoglobin by specific covalent modification (acetylation and crosslinking) of this protein but do not interfere with oxygen transport. These compounds were toxic to malaria parasites when continuously present in culture, as were drugs with similar pharmacological effects such as indomethacin, ibuprofen, and phenylbutazone. Aspirin and acetaminophen were much less effective. When erythrocytes were pretreated with these compounds prior to parasite exposure, only dibromoaspirin and dibromosalicyl diesters prevented parasite development. The modified hemoglobin was highly resistant to digestion by cathepsin D and parasite proteases, suggesting that covalent modifications of hemoglobin that do not disrupt normal hemoglobin function have antimalarial effects.
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PMID:Inhibition of the growth of Plasmodium falciparum in vitro by covalent modification of hemoglobin. 636 46


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