Together withomega−3 fatty acids and other omega−6 fatty acids, arachidonic acid provides energy for body functions, contributes tocell membrane structure, and participates in the synthesis ofeicosanoids, which have numerous roles in physiology assignaling molecules.[2][5]
Some chemistry sources define 'arachidonic acid' to designate any of theeicosatetraenoic acids. However, almost all writings in biology, medicine, and nutrition limit the term toall cis-5,8,11,14-eicosatetraenoic acid.
In addition to being involved incellular signaling as a lipidsecond messenger involved in the regulation of signaling enzymes, such asPLC-γ, PLC-δ, andPKC-α, -β, and -γ isoforms, arachidonic acid is a key inflammatory intermediate and can also act as avasodilator.[8] (Note separate synthetic pathways, as described in section below.)
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 ofeicosanoids:
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 to15-hydroxyeicosatetraenoic acid (15-HETE) andlipoxins;[12][13][14] 15-Lipoxygenase-1 may also further metabolize 15-HPETE toeoxins 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 to12-hydroxyeicosatetraenoic acid (12-HETE) and tohepoxilins.[16]
The production of these derivatives and their actions in the body are collectively known as the "arachidonic acid cascade"; seeEssential fatty acid interactions and the enzyme and metabolite linkages given in the previous paragraph for more details.
Along with other omega−6 and omega−3 fatty acids, arachidonic acid contributes to the structure of cell membranes.[2] When incorporated intophospholipids, 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 todocosahexaenoic 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]
This sectionis missing information about Typical dietary intake — needed to put supplement dose into context. Please expand the section to include this information. Further details may exist on thetalk page.(February 2025)
Arachidonic acid is marketed as adietary 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 noadverse effects in adults of using high daily doses (1500 mg) of arachidonic acid on severalbiomarkers ofblood chemistry,immune function, andinflammation.[23]
A 2009 review indicated that consumption of 5−10% offood energy from omega−6 fatty acids including arachidonic acid may reduce the risk ofcardiovascular 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]
^Smith WL, Song I (2002). "The enzymology of prostaglandin endoperoxide H synthases-1 and -2".Prostaglandins & Other Lipid Mediators.68–69:115–28.doi:10.1016/s0090-6980(02)00025-4.PMID12432913.
^Romano M, Cianci E, Simiele F, Recchiuti A (Aug 2015). "Lipoxins and aspirin-triggered lipoxins in resolution of inflammation".Eur J Pharmacol.760:49–63.doi:10.1016/j.ejphar.2015.03.083.PMID25895638.
^Porro B, Songia P, Squellerio I, Tremoli E, Cavalca V (Aug 2014). "Analysis, physiological and clinical significance of 12-HETE: A neglected platelet-derived 12-lipoxygenase product".J Chromatogr B.964:26–40.doi:10.1016/j.jchromb.2014.03.015.PMID24685839.
^Walter F., PhD. Boron (2003).Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. p. 108.ISBN1-4160-2328-3.
^abcdefWalter F., PhD. Boron (2003).Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. p. 103.ISBN1-4160-2328-3.
^abcdefWalter F., PhD. Boron (2003).Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. p. 104.ISBN1-4160-2328-3.
^Crawford MA, Sinclair AJ (1971).Nutritional influences in the evolution of mammalian brain. In: lipids, malnutrition & the developing brain. pp. 267–92.doi:10.1002/9780470719862.ch16.PMID4949878.{{cite book}}:|journal= ignored (help)
