Damage to malaria-infected erythrocytes following exposure to oxidant-generating systems

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Abstract
A study has been made of the damage incurred by normal and Plasmodium falciparum-infected human erythrocytes following exposure to a variety of oxidant-generating systems. Hydrogen peroxide, produced by the glucose–glucose oxidase system, increased methaemoglobin formation within normal erythrocytes while normal levels of oxyhaemoglobin were maintained. Exposure to products of the xanthine–xanthine oxidase interaction did not have the same effect. Malondialdehyde measurements indicated that the host cell membranes of parasitized cells had undergone lipid peroxidation even before exposure to the oxidant-generating systems. Lipid peroxidation of normal and parasitized cell membranes was increased upon exposure to reagent-grade hydrogen peroxide and alloxan: this increase was not observed following exposure to the two enzyme–substrate systems that generated reactive oxygen intermediates. In addition, the effects of parasitism on intracellular levels of catalase and superoxide dismutase were assessed. Normal and parasitized erythrocytes were found to possess similar levels of these enzymes, which protect against oxidant-induced damage. It was therefore concluded that the increased susceptibility of infected cells to oxidant damage was probably not related to any decrease in the function of these enzymes.