Lipoxin Generation in Human Whole Blood: Monitoring by Electron-Capture NICI GC/MS

Abstract

Mammalian lipoxygenase-derived products of arachidonic acid were first identified with cells of hematopoietic origins (reviewed in ref. 1). Products of these enzymatic pathways (e.g. leukotrienes) play critical roles in a wide range of physiologic responses (2). The lipoxins (LX) are an addition to the established family of bioactive eicosanoids. Members of the LX series contain a conjugated tetraene structure, can be generated by the interactions of individual lipoxygenases or by cell-cell interactions, and display a profile of bioactions unique among eicosanoids (reviewed in 2,3). Results from several laboratories now show that lipoxin A₄ can block the proinflammatory actions of leukotriene B₄ and the hemodynamic effects of leukotriene D₄. LXA₄ may also play an intracellular role in its cell of origin, since it activates isolated protein kinase C and has been found to inhibit IP₃ formation (recently reviewed in ref. 3). Thus, as is the case with other bioactive eicosanoids, the availability of appropriate quantitative methods will play a critical role in assessing the temporal association between lipoxin formation and their potential involvement in both physiologic and pathophysiologic events.