title: Impact of EPA ingestion on COX- and LOX-mediated eicosanoid synthesis in skin with and without a pro-inflammatory UVR challenge--report of a randomised controlled study in humans.
abstract: METHODS
  Eicosapentaenoic acid (EPA), abundant in oily fish, is reported to reduce skin inflammation and provide photoprotection, potential mechanisms include competition with arachidonic acid (AA) for metabolism by cyclooxygenases/lipoxygenases to less pro-inflammatory mediators. We thus examine impact of EPA intake on levels of AA, EPA and their resulting eicosanoids in human skin with or without ultraviolet radiation (UVR) challenge.
  
  
  RESULTS
  In a double-blind randomised controlled study, 79 females took 5 g EPA-rich or control lipid for 12 wk. Pre- and post-supplementation, red blood cell and skin polyunsaturated fatty acids were assessed by GC, and eicosanoids from unexposed and UVR-exposed skin by LC-MS/MS. Active supplementation increased red blood cell and dermal EPA versus control (both p < 0.001), lowering relative AA:EPA content (4:1 versus 15:1 and 5:1 versus 11:1, respectively; both p < 0.001). Pre-supplementation, UVR increased PGE2, 12-hydroxyeicosatetraenoic acids, 12-HEPE (all p < 0.001) and PGE3 (p < 0.05). Post-EPA, PGE2 was reduced in unchallenged skin (p < 0.05) while EPA-derived PGE3 (non-sign) and 12-HEPE (p < 0.01) were elevated post-UVR. Thus, post-EPA, PGE2 :PGE3 was lower in unchallenged (12:1 versus 28:1; p < 0.05) and UVR exposed (12:1 versus 54:1; p < 0.01) skin; 12-hydroxyeicosatetraenoic acids:12-HEPE was lower in UVR-exposed skin (3:1 versus 11:1; p < 0.001).
  
  
  CONCLUSIONS
  Dietary EPA augments skin EPA:AA content, shifting eicosanoid synthesis towards less pro-inflammatory species, and promoting a regulatory milieu under basal conditions and in response to inflammatory insult.
authors: Dermatology Centre, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Hospital, University of Manchester, Manchester, UK.
authors: Suzanne M
authors: SM
authors: Pilkington
authors: Lesley E
authors: LE
authors: Rhodes
authors: Naser M I
authors: NM
authors: Al-Aasswad
authors: Karen A
authors: KA
authors: Massey
authors: Anna
authors: A
authors: Nicolaou
mesh_terms: D019377:12-Hydroxy-5,8,10,14-eicosatetraenoic Acid / Q000378:metabolism; D000328:Adult; D000527:Alprostadil / Q000031:analogs & derivatives / Q000378:metabolism; D016718:Arachidonic Acid / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D015777:Eicosanoids / Q000096:biosynthesis*; D015118:Eicosapentaenoic Acid / Q000378:metabolism / Q000494:pharmacology*; D004890:Erythema / Q000178:diet therapy / Q000209:etiology; D005260:Female; D006801:Humans; D008084:Lipoxygenase / Q000378:metabolism; D008875:Middle Aged; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000528:radiation effects; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D015777:Eicosanoids; D016718:Arachidonic Acid; D019377:12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; C033246:prostaglandin E3; D015118:Eicosapentaenoic Acid; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases; D000527:Alprostadil; D015232:Dinoprostone
keywords: 12-HETE; EPA; Inflammation; PGE2; UVR