Lipids in Health and Disease · 2 authors, 2 centres
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Mead acid (MA) is an endogenous n-9 polyunsaturated fatty acid that is synthesized de novo and distributed in various normal tissues, not only in essential fatty acid deficiency. MA can be converted into unique lipid mediators and competes with arachidonic acid, influencing inflammation, cancer, dermatitis, and cystic fibrosis. This review highlights MA's potential as a multifunctional PUFA with clinical significance in disease modulation.
**Background:** Mead acid (MA, 5,8,11-eicosatrienoic acid) is an n-9 polyunsaturated fatty acid (PUFA) first identified in rats fed a fat-deficient diet. It is synthesized from oleic acid via the same enzyme system as n-6 and n-3 PUFAs, but its formation is suppressed in the presence of linoleic acid (LA) and α-linolenic acid (ALA). MA is widely used as a marker of essential fatty acid (EFA) deficiency, but recent studies suggest it has active physiological and pathological roles. This narrative review summarizes the biosynthesis, presence, metabolism, and disease associations of MA.
**Methods:** The authors conducted a narrative review of the literature on MA, covering its biosynthesis, distribution in tissues, metabolism to lipid mediators, and associations with inflammation, cancer, dermatitis, cystic fibrosis, and other diseases. Studies included animal models, cell culture experiments, and human epidemiological data. The review does not specify a systematic search strategy or inclusion criteria.
**Key Results:** MA is present in various normal tissues of healthy adults, including plasma (0.16%), serum (0.24%), blood vessels (0.1%), and liver (0.2%). Higher levels are found in fetal tissues (e.g., plasma 0.44%, blood vessels 2.4%) and avascular tissues like cartilage (up to 16.98% in chicken) and lens (3.19% in calf). MA can be absorbed from the digestive tract and distributed to tissues, reaching levels above 20% in some studies. It is metabolized by 5-lipoxygenase (5-LOX) to 3-series leukotrienes (e.g., LTC3, LTD3, LTE3, LTB3) and by cyclooxygenase (COX) to 13-HETrE and other metabolites. MA-derived 5-oxo-ETrE activates granulocytes similarly to 5-oxo-ETE. In inflammation studies, dietary MA supplementation in rats inhibited LTB4 synthesis in neutrophils and suppressed platelet-activating factor generation in mice. In cancer, MA inhibited growth of KPL-1 human breast cancer cells in vitro and in vivo, and suppressed mammary carcinogenesis in rats. A nested case-control study found that plasma MA composition was inversely associated with overall cancer risk and breast cancer risk. In dermatitis, topical MA caused scaly dermatitis in hairless mice, but intraperitoneal MA inhibited contact hypersensitivity in mice. In cystic fibrosis, increased MA and decreased EFAs are observed in serum. Other findings include MA incorporation into platelets, suppression of osteoblastic activity, and association with fibrosis stage 3-4 in nonalcoholic fatty liver disease.
**Clinical Implications:** MA is an endogenous PUFA with diverse biological activities, including modulation of inflammation, cancer, and dermatitis. Its ability to compete with arachidonic acid and produce unique lipid mediators suggests potential therapeutic applications. However, the evidence is limited by the narrative review approach and the small number of supporting studies. Further research is needed to clarify MA's role in disease and its potential as a therapeutic target.