Arachidonic acid 5-hydroperoxide
Arachidonic acid 5-hydroperoxide leukotriene A4 which is then metabolized to the chemotactic factor for leukocytes, leukotriene B4, or to contractors of lung airways, leukotriene C4, leukotriene D4, and leukotriene E4; b) the leukocyte chemotactic factors, 5-hydroxyicosatetraenoic acid and 5-oxo-eicosatetraenoic acid; or c) the specialized pro-resolving mediators of inflammation, lipoxin A4 and lipoxin B4.
Image:Eicosanoid synthesis.svg|thumb|center|320px|Eicosanoid synthesisThe 5-LOX catalyzed product, 5-HPETE, is capable of restoring a suppressed macrophages only when the natural killer cell activity becomes deactivated. Fatty acids typically weaken some pro-inflammatory mechanism driven by arachidonic acid. When Eicosapentaenoic acid, a omega-3 fatty acid, competes with arachidonic acid for the enzyme binding sites, less arachidonic acid derivatives are produce. In this case, macrophage failed to activate NK cells. Studies have found that by adding 5-HPETE to the EPA-suppressed macrophages in rats will remove and replace EPA from 5-LOX binding site to restore the function of its ability to activate the NK cell signaling.