Glucose-6-phosphate dehydrogenase (G6PD) !

G6PD makes NADPH in the pentose pathway; in the red blood cell it is the only defence against oxidative damage.

Updated 2026-11-01

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Key facts

Glucose 6-phosphate + NADP⁺ → 6-phosphogluconolactone + NADPH: the rate-limiting step of the pentose phosphate pathway.
The gene is on the X chromosome: deficiency mainly affects males; heterozygous women have variable activity.
Besides the catalytic NADP⁺, each subunit has a structural NADP⁺ that stabilises it; many severe variants disturb that site.
Deficiency gives partial protection against P. falciparum malaria, which explains its high frequency in malarial areas.

NADP⁺ activates it and NADPH inhibits it.
Insulin and a carbohydrate-rich diet increase its synthesis in liver and adipose tissue.

G6PD deficiency causes acute haemolysis after fava beans, infections or oxidant drugs (primaquine, tafenoquine, dapsone, rasburicase, some sulfonamides).
In Colombia, where P. vivax malaria is treated with primaquine, G6PD testing matters before that treatment.
The smear shows Heinz bodies (oxidised haemoglobin) and bite cells.

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Why does G6PD deficiency mainly affect the red cell?

The red cell has no mitochondria or other NADPH source; without it, it cannot regenerate reduced glutathione.

How is G6PD deficiency inherited?

X-linked recessive: mainly men are affected.

Which antimalarial requires knowing G6PD status before it is given?

Primaquine (and tafenoquine), which can cause severe haemolysis in deficient people.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: G6PD: Glucose-6-phosphate 1-dehydrogenase (human) (UniProt, 2026); G6PD gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); 2BHL: X-RAY STRUCTURE OF HUMAN GLUCOSE-6-PHOSPHATE DEHYDROGENASE (DELETION VARIANT) COMPLEXED WITH GLUCOSE-6-PHOSPHATE (RCSB Protein Data Bank, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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