In chemical structure, arachidonic acid is a carboxylic acid with a 20-carbon chain and four cis-double bonds; the first double bond is located at the sixth carbon from the omega end.

Some chemistry sources define 'arachidonic acid' to designate any of the eicosatetraenoic acids. However, almost all writings in biology, medicine, and nutrition limit the term to all cis-5,8,11,14-eicosatetraenoic acid.

Arachidonic acid is a polyunsaturated fatty acid present in the phospholipids (especially phosphatidylethanolamine, phosphatidylcholine, and phosphatidylinositides) of membranes of the body's cells, and is abundant in the brain, muscles, and liver. Skeletal muscle is an especially active site of arachidonic acid retention, accounting for roughly 10–20% of the phospholipid fatty acid content typically.^[7]

In addition to being involved in cellular signaling as a lipid second messenger involved in the regulation of signaling enzymes, such as PLC-γ, PLC-δ, and PKC-α, -β, and -γ isoforms, arachidonic acid is a key inflammatory intermediate and can also act as a vasodilator.^[8] (Note separate synthetic pathways, as described in section below.)

Arachidonic acid is freed from phospholipid by hydrolysis, catalyzed by the phospholipase A₂ (PLA₂).^[8]

Arachidonic acid for signaling purposes appears to be derived by the action of group IVA cytosolic phospholipase A₂ (cPLA₂, 85 kDa), whereas inflammatory arachidonic acid is generated by the action of a low-molecular-weight secretory PLA₂ (sPLA₂, 14-18 kDa).^[8]

Arachidonic acid is a precursor to a wide range of eicosanoids:

• The enzymes cyclooxygenase-1 and -2 (i.e. prostaglandin G/H synthase 1 and 2 [⁠PTGS1 and PTGS2]) convert arachidonic acid to prostaglandin G₂ and prostaglandin H₂, which in turn may be converted to various prostaglandins, to prostacyclin, to thromboxanes, and to the 17-carbon product of thromboxane metabolism of prostaglandin G₂/H₂, 12-hydroxyheptadecatrienoic acid (12-HHT).^[9][10]
• The enzyme 5-lipoxygenase catalyzes the oxidation of arachidonic acid to 5-hydroperoxyeicosatetraenoic acid (5-HPETE), which in turn converts to various leukotrienes (i.e., leukotriene B₄, leukotriene C₄, leukotriene D₄, and leukotriene E₄) as well as to 5-hydroxyeicosatetraenoic acid (5-HETE) which may then be further metabolized to 5-HETE's more potent 5-keto analog, 5-oxo-eicosatetraenoic acid (5-oxo-ETE) (also see 5-hydroxyeicosatetraenoic acid).^[11]
• The enzymes 15-lipoxygenase-1 (ALOX15) and 15-lipoxygenase-2 (ALOX15B). ALOX15B catalyzes the oxidation of arachidonic acid to 15-hydroperoxyeicosatetraenoic acid (15-HPETE), which may then be further converted to 15-hydroxyeicosatetraenoic acid (15-HETE) and lipoxins;^[12][13][14] 15-Lipoxygenase-1 may also further metabolize 15-HPETE to eoxins in a pathway analogous to (and presumably using the same enzymes as used in) the pathway which metabolizes 5-HPETE to leukotrienes.^[15]
• The enzyme 12-lipoxygenase (ALOX12) catalyzes oxidation of arachidonic acid to 12-hydroperoxyeicosatetraenoic acid (12-HPETE), which may then be metabolized to 12-hydroxyeicosatetraenoic acid (12-HETE) and to hepoxilins.^[16]
• Arachidonic acid is also a precursor to anandamide.^[17]
• Some arachidonic acid is converted into hydroxyeicosatetraenoic acids (HETEs) and epoxyeicosatrienoic acids (EETs) by epoxygenase.^[18]

The production of these derivatives and their actions in the body are collectively known as the "arachidonic acid cascade"; see Essential fatty acid interactions and the enzyme and metabolite linkages given in the previous paragraph for more details.

PLA₂, in turn, is activated by ligand binding to receptors, including:

• 5-HT2 receptors ^[19]
• mGLUR1^[19]
• bFGF receptor^[19]
• IFN-α receptor^[19]
• IFN-γ receptor^[19]

Furthermore, any agent increasing intracellular calcium may cause activation of some forms of PLA₂.^[20]

Alternatively, arachidonic acid may be cleaved from phospholipids after phospholipase C (PLC) cleaves off the inositol trisphosphate group, yielding diacylglycerol (DAG), which subsequently is cleaved by DAG lipase to yield arachidonic acid.^[19]

Receptors that activate this pathway include:

• A₁ receptor^[20]
• D₂ receptor^[20]
• α₂ adrenergic receptor^[20]
• 5-HT1 receptor^[20]

PLC may also be activated by MAP kinase. Activators of this pathway include PDGF and FGF.^[20]

Along with other omega−6 and omega−3 fatty acids, arachidonic acid contributes to the structure of cell membranes.^[2] When incorporated into phospholipids, the omega fatty acids affect cell membrane properties, such as permeability and the activity of enzymes and cell-signaling mechanisms.^[2]

Arachidonic acid, one of the most abundant fatty acids in the brain, is present in similar quantities to docosahexaenoic acid, with the two accounting for about 20% of brain fatty-acid content.^[21] Arachidonic acid is involved in the early neurological development of infants.^[22]

Arachidonic acid is marketed as a dietary supplement.^[2][5] A 2019 review of clinical studies investigating the potential health effects of arachidonic acid supplementation of up to 1500 mg per day on human health found there were no clear benefits.^[23] There were no adverse effects in adults of using high daily doses (1500 mg) of arachidonic acid on several biomarkers of blood chemistry, immune function, and inflammation.^[23]

A 2009 review indicated that consumption of 5−10% of food energy from omega−6 fatty acids including arachidonic acid may reduce the risk of cardiovascular diseases compared to lower intakes.^[24] A 2014 meta-analysis of possible associations between heart disease risk and individual fatty acids reported a significantly reduced risk of heart disease with higher levels of EPA, DHA, and arachidonic acid.^[25]

• Arachidonic+Acid at the U.S. National Library of Medicine Medical Subject Headings (MeSH)