Biochemistry · Enzyme
Glutathione peroxidase (GPX) !
Glutathione peroxidase removes hydrogen peroxide and lipid peroxides using glutathione; it contains selenium.
Updated 2026-11-01
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Key facts
- H₂O₂ + 2 GSH → 2 H₂O + GSSG; it also reduces lipid peroxides to alcohols.
- Its active site has selenocysteine: dietary selenium is essential.
- Glutathione reductase regenerates GSH with NADPH, which in red cells comes only from the pentose phosphate pathway (G6PD).
- GPX4 protects membranes from peroxidation; when it fails, the cell dies by ferroptosis.
Regulation
- It depends on GSH and NADPH supply (G6PD).
- Its activity falls with selenium deficiency.
Inhibitors and toxins
- ML162 and RSL3 (GPX4, experimental; they trigger ferroptosis)
Clinical notes
- In G6PD deficiency NADPH is lacking, GSH is not regenerated and oxidants (drugs, fava beans, infections) cause hemolysis.
- Severe selenium deficiency is linked to cardiomyopathy (Keshan disease).
- The 3D view shows human GPX4 bound to the inhibitor ML162 in the active site (structure 6HKQ).
Related
Test yourself
Think of the answer, then tap the question to see it.
Which trace element does glutathione peroxidase need?
Selenium, as selenocysteine in the active site.
Why does G6PD deficiency leave red cells defenceless against H₂O₂?
Without G6PD there is no NADPH; glutathione reductase cannot regenerate GSH and glutathione peroxidase runs out of substrate.
Which form of cell death appears when GPX4 fails?
Ferroptosis, from iron-dependent build-up of lipid peroxides.
Educational information, not medical advice. For any symptom, see a health professional.
Sources: GPX1: Glutathione peroxidase 1 (human) (UniProt, 2026); GPX4: Phospholipid hydroperoxide glutathione peroxidase GPX4 (human) (UniProt, 2026); Detoxification of Reactive Oxygen Species (Reactome, 2026); 6HKQ: Human GPX4 in complex with covalent Inhibitor ML162 (S enantiomer) (RCSB Protein Data Bank, 2026).
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Representative model, for educational purposes only.