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indeed, with respect to malaria protection, it has been theorized that protection conferred by G6PD deficiency may be related to increased phagocytosis of parasitized oxidatively-damaged G6PD-deficient RBCs (7779) via binding by macrophage Fc and lectin-like receptors (80), and that such parasites may be more susceptible to ROS (81)

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6b) is more efficient than the formation of the transition state between the glutathionylated enzyme and GSH (Fig