eicosanoider

Eicosanoids are bioactive lipid mediators derived from twenty-carbon fatty acids, principally arachidonic acid. They function as local signaling molecules that regulate inflammatory responses, vascular tone, pain, and hemostasis.

Most eicosanoids are produced on demand from membrane phospholipids by phospholipase A2, which liberates arachidonic acid. The two main enzymatic routes are the cyclooxygenase (COX) pathway, yielding prostaglandins, prostacyclin (PGI2), and thromboxanes (TXA2), and the lipoxygenase (LOX) pathway, generating leukotrienes and lipoxins. A separate cytochrome P450 pathway produces epoxyeicosatrienoic acids (EETs). The various products act through specific receptors, many of which are G protein–coupled, to induce diverse responses.

Major eicosanoids include prostaglandins (for example PGE2, PGD2, PGF2α) that regulate fever, pain, vasodilation, and vascular permeability; prostacyclin (PGI2) and thromboxane (TXA2) control platelet aggregation and vascular tone; leukotrienes (LTB4, LTC4, LTD4, LTE4) promote chemotaxis, edema, and bronchoconstriction; lipoxins participate in the resolution of inflammation.

Because they act locally and are rapidly inactivated, eicosanoids link dietary fatty acids to inflammatory states. Arachidonic acid is derived from omega-6 fatty acids, while eicosanoids from omega-3 fatty acids (e.g., EPA, DHA) tend to be less inflammatory or anti-inflammatory.

Pharmacologically, NSAIDs inhibit COX, reducing prostaglandin production; corticosteroids suppress phospholipase A2; leukotriene inhibitors and receptor antagonists are used in asthma and allergic conditions. Eicosanoids thus play central roles in physiology and disease.