Mj. Griffiths et al., Oxidative stress and erythrocyte damage in Kenyan children with severe Plasmodium falciparum malaria, BR J HAEM, 113(2), 2001, pp. 486-491
Anaemia causes significant morbidity in children with Plasmodium falciparum
malaria, but the mechanism(s) are unclear. During malarial infection, incr
eased reactive oxygen species (ROS) are generated that may contribute to er
ythrocyte damage and anaemia. This study measured the concentrations of alp
ha -tocopherol in plasma and erythrocyte membranes, and the percentage poly
unsaturated fatty acid composition (%PUFA) (an indirect marker of ROS damag
e) in erythrocyte membranes in children with severe P. falciparum malaria f
rom Kilifi, Kenya, and asymptomatic children from the same district. Malari
al subjects were stratified Into complicated malaria and malaria anaemia. R
esults demonstrated significant reductions in erythrocyte membrane cli-toco
pherol concentration (1.63 +/- 0.16 versus 3.38 +/- 0.18 mu mol/mg protein;
P<0.001) and total %PUFA (30.7 +/- 0.49 versus 32.8 +/- 0.44% P < 0.005) f
or the malarial subjects (non-stratified) compared with controls. Malarial
subjects showed a significant positive correlation between membrane alpha -
tocopherol and haemoglobin concentrations (P < 0.005 r = 0.63 complicated m
alaria group; P < 0.05 r = 0.36 non-stratified data). There were no signifi
cant differences in plasma alpha -tocopherol concentration between malaria
patients and controls. In conclusion, malarial infection may be associated
with oxidative damage and reduced alpha -tocopherol reserve in the erythroc
yte membrane, suggesting that local antioxidant depletion may contribute to
erythrocyte loss in severe malaria. Erythrocyte membrane alpha -tocopherol
appeared a better indicator of ROS exposure than plasma.