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Killing of blood-stage Plasmodium falciparum by lipid peroxides from tumor necrosis serum.

Abstract
The multiplication of Plasmodium falciparum in culture, as measured by [3H]hypoxanthine incorporation, was inhibited in a dose-dependent manner by rabbit tumor necrosis serum. The regimen by which tumor necrosis serum is produced caused significant increases in the levels of triglycerides and lipid peroxides, with the latter being indicated by the level of malondialdehyde in the serum. When tumor necrosis serum was depleted of lipoproteins by aerosil (fumed silica), no parasiticidal activity remained, and when it was separated by ultracentrifugation, more than 70% of the parasiticidal activity was found in the lipoprotein fraction. This suggests that lipid peroxides may account for most of the parasiticidal activity in tumor necrosis serum but that a nonlipid toxic factor may also be present.
AuthorsK A Rockett, G A Targett, J H Playfair
JournalInfection and immunity (Infect Immun) Vol. 56 Issue 12 Pg. 3180-3 (Dec 1988) ISSN: 0019-9567 [Print] United States
PMID3053454 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Lipid Peroxides
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
Topics
  • Animals
  • Dose-Response Relationship, Drug
  • In Vitro Techniques
  • Lipid Peroxides (toxicity)
  • Lipopolysaccharides (pharmacology)
  • Mycobacterium bovis (immunology)
  • Plasmodium falciparum (drug effects)
  • Rabbits
  • Tumor Necrosis Factor-alpha (pharmacology)

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