Oxidative stress and erythrocyte damage in Kenyan children with severe Plasmodium falciparum malaria

Anaemia causes significant morbidity in children with Plasmodium falciparum malaria, but the mechanism(s) are unclear. During malarial infection, increased reactive oxygen species (ROS) are generated that may contribute to erythrocyte damage and anaemia. This study measured the concentrations of α‐tocopherol in plasma and erythrocyte membranes, and the percentage polyunsaturated fatty acid composition (%PUFA) (an indirect marker of ROS damage) in erythrocyte membranes in children with severe P. falciparum malaria from Kilifi, Kenya, and asymptomatic children from the same district. Malarial subjects were stratified into complicated malaria and malaria anaemia. Results demonstrated significant reductions in erythrocyte membrane α‐tocopherol concentration (1·63 ± 0·16 versus 3·38 ± 0·18 μmol/mg protein; P < 0·001) and total %PUFA (30·7 ± 0·49 versus 32·8 ± 0·44% P < 0·005) for the malarial subjects (non‐stratified) compared with controls. Malarial subjects showed a significant positive correlation between membrane α‐tocopherol and haemoglobin concentrations (P < 0·005 r = 0·63 complicated malaria group; P < 0·05 r = 0·36 non‐stratified data). There were no significant differences in plasma α‐tocopherol concentration between malaria patients and controls. In conclusion, malarial infection may be associated with oxidative damage and reduced α‐tocopherol reserve in the erythrocyte membrane, suggesting that local antioxidant depletion may contribute to erythrocyte loss in severe malaria. Erythrocyte membrane α‐tocopherol appeared a better indicator of ROS exposure than plasma.