Eoxins are proposed to be a family of proinflammatory eicosanoids (signaling compounds that regulate inflammatory and immune responses).
[2][3] A closely related set of 15-lipoxygenase metabolites are derived from anandamide (i.e. arachidonic acid containing ethanolamine esterified to its carboxy residue).
These eoxin-like metabolites, termed eoxamides, are also formed by L1235 Reed-Sternberg cells and proposed to play a role in Hodgkins disease.
[2] Furthermore, Eoxins stimulate vascular permeability in an ex vivo human vascular endothelial model system,[2] and in a small study of 32 volunteers EXC4 production by eosinophils isolated from severe and aspirin-intolerant asthmatics was greater than that from healthy volunteers and mild asthmatic patients.
A subsequent study found that eoxin levels in the exhaled breath of aspirin-sensitive and aspirin-intolerant asthmatic individuals did not rise after aspirin challenge and did not correlate with disease severity.
[3] The same pathways that metabolize arachidonic acid to eoxines have been shown to metabolize anandamide, N-arachidonoylethanolamine (i.e. arachidonic acid containing ethanolamine esterified to its carboxy residue) into a set of eoxamides that are identical to their eoxin counterparts except that they possess an ethanolamine ester.