Killing of blood-stage Plasmodium falciparum by lipid peroxides from tumor necrosis serum.
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.
D000818:Animals; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D008054:Lipid Peroxides / Q000633:toxicity*; D008070:Lipopolysaccharides / Q000494:pharmacology; D009163:Mycobacterium bovis / Q000276:immunology; D010963:Plasmodium falciparum / Q000187:drug effects*; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D008054:Lipid Peroxides; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha