Redox metabolism of vitamin C in blood of normal and malaria-infected mice

Abstract

As oxidative mechanisms have been suggested to be part of the host immune reaction against malarial parasites, we investigated the redox metabolism of the antioxidant vitamin C in the blood of control and malaria-infected mice. At the peak of infection (day 6) with the malaria parasite P. vinckei, plasma levels of ascorbate (AH −) were 10.8 ± 0.9 μg/ml compared to 5.7 ± 0.7 μg/ml in control mice, though no significant change was observed in the plasma concentration of dehydroascorbate (DHA). The plasma redox ratio of vitamin C, [AH −]:[DHA], was 7.4 in control mice and 18.5 in infected mice on day 6 post-inoculation. The increased AH − level in plasma of P. vinckei-infected mice was not due to differences in stabilities of either AH − or DHA in plasmas from control or P. vinckei-infected mice. DHA added to plasma was lost rapidly. In contrast, when added to whole blood, DHA was rapidly taken up and reduced to AH − by blood cells from both normal mice and P. vinckei-infected mice. Most of the intracellular AH − derived from the exogenously added DHA was released into the plasma by blood cells from the infected but not normal mice. The observed release of AH − into the plasma by blood cells from infected mice was not caused by a plasma factor. Depletion of leukocytes from erythrocytes had no effect on the uptake and reduction of DHA by red blood cells, but the subsequent release of intracellular AH − occurred more rapidly. The increased propensity of erythrocytes from infected animals to release AH − could in part explain the higher levels of AH − observed in P. vinckei infection.