Abstract
Glucose-6-phosphate-dehydrogenase (G6PD) catalyzes the first step in the hexose monophosphate (HMP) shunt. This pathway serves to supply the cell with NADPH, the most important function being probably the maintainance of glutathione (GSH) in the reduced state. G6PD deficiency is the most common disease-producing enzyme deficiency of human beings, affecting about one hundred million people throughout the world. G6PD is subject to different mutations, and more than two hundred variants have been reported. Some of these cause a deficiency of enzyme activity in erythrocytes, leading to hemolitic anemia, usually upon exposure to an offending drug or toxin. Hemolysis may also occur during infection, diabetic acidosis, or when there is no known inciting cause. Some persons, perhaps carrying an additional genetic defect, show a particular sensitivity to fava beans (favism), whether upon ingestion or exposure to pollen. Different genetic variants of G6PD may have effects in tissues other than the erythrocytes, including the CNS.
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Bocchetta, A., Del Zompo, M., Corsini, G.U. (1990). Glucose-6-phosphate dehydrogenase deficiency and psychoses. In: Cazzullo, C.L., Sacchetti, E., Conte, G., Invernizzi, G., Vita, A. (eds) Plasticity and Morphology of the Central Nervous System. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0851-2_21
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DOI: https://doi.org/10.1007/978-94-009-0851-2_21
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