Eicosanoids: prostaglandins, thromboxanes and leukotrienes !

Eicosanoids are local messengers made from arachidonic acid: they control inflammation, pain, fever, clotting and airways.

Updated 2026-11-01

Key facts

Phospholipase A₂ releases arachidonic acid (20 C, ω-6) from membranes; corticosteroids restrain it.
Cyclooxygenase (COX-1/COX-2) branch: PGH₂ → prostaglandins, prostacyclin (PGI₂) and thromboxane A₂ (TXA₂).
5-Lipoxygenase branch: LTB₄ (attracts neutrophils) and LTC₄/D₄/E₄ (bronchoconstriction, leaky vessels).
Aspirin acetylates COX irreversibly; in the anucleate platelet the antiplatelet effect lasts its lifespan (7–10 days).
TXA₂ (platelet) aggregates and constricts vessels; PGI₂ (endothelium) does the opposite.

1. A stimulus (injury, cytokines) activates phospholipase A₂, which cuts arachidonate from phospholipids.
2. COX performs two reactions: cyclooxygenase (forms PGG₂) and peroxidase (PGH₂).
3. Each tissue converts PGH₂ according to its enzymes: thromboxane in platelets, prostacyclin in endothelium, PGE₂ and PGF₂α in many tissues.
4. 5-Lipoxygenase, with its activating protein (FLAP), forms LTA₄, which gives LTB₄ and the cysteinyl leukotrienes.
5. NSAIDs block COX; coxibs mainly COX-2; zileuton inhibits 5-lipoxygenase and montelukast blocks the cysteinyl-leukotriene receptor.
6. ω-3 fatty acids (EPA) give series-3 eicosanoids, which are less inflammatory and less pro-aggregant.

PGE₂ protects the gastric mucosa: that is why NSAIDs promote peptic ulcer.
In the newborn, COX inhibitors close a patent ductus arteriosus and PGE₁ keeps it open.
Cysteinyl leukotrienes cause bronchoconstriction in asthma; aspirin can trigger asthma in sensitive people.
Uterine prostaglandins (PGF₂α, PGE₂) explain dysmenorrhoea and its response to NSAIDs.

Think of the answer, then tap the question to see it.

Why does aspirin's antiplatelet effect last the platelet's whole life?

Aspirin acetylates COX irreversibly and the anucleate platelet cannot make new enzyme.

Which eicosanoid attracts neutrophils?

Leukotriene B₄ (LTB₄).

Which enzyme do corticosteroids restrain to lower all eicosanoids?

Phospholipase A₂ (via lipocortin/annexin A1), which releases arachidonic acid.

Which prostanoids have opposite effects on platelet aggregation?

Thromboxane A₂ (platelets) promotes it and prostacyclin PGI₂ (endothelium) inhibits it.

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

Sources: Arachidonate metabolism (Reactome, 2026); Synthesis of Prostaglandins (PG) and Thromboxanes (TX) (Reactome, 2026); Synthesis of Leukotrienes (LT) and Eoxins (EX) (Reactome, 2026); Prostaglandin E2 (CID 5280360) (PubChem, NCBI, 2026) · Public domain; Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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Representative model, for educational purposes only.