Protection of vitamin E from oxidation by increased ascorbic acid content within Plasmodium vinckei-infected erythrocytes.
Erythrocytes isolated from mice at a late stage of infection with the malarial parasite Plasmodium vinckei contained increased levels of vitamin E, but neither control nor infected erythrocytes contained detectable levels of alpha-tocopherolquinone, an oxidation product of vitamin E. Total levels of the antioxidant, vitamin C, were more than doubled in the same populations of highly parasitized erythrocytes. These observations, and the lower ratio of oxidized to reduced forms of ascorbic acid in parasitized compared to nonparasitized erythrocytes, raise the possibility that increased redox-cycling between the two vitamins may account for the failure to detect alpha-tocopherolquinone. Thus, late in infection of mice with the lethal parasite P. vinckei, the content and redox state of erythrocytic ascorbic acid is altered so that it protects vitamin E, and presumably the parasitized red cell and its contents, from oxidative damage.
D000818:Animals; D001205:Ascorbic Acid / Q000097:blood*; D002851:Chromatography, High Pressure Liquid; D004912:Erythrocytes / Q000378:metabolism*; D007700:Kinetics; D008288:Malaria / Q000097:blood*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010084:Oxidation-Reduction; D010961:Plasmodium / Q000472:pathogenicity*; D014810:Vitamin E / Q000097:blood*
D014810:Vitamin E; D001205:Ascorbic Acid