Arachidonic acid is released from membrane phospholipids upon cell stimulation (for example, by immune complexes and calcium ionophores) and converted to leukotrienes by a 5-lipoxygenase that also has leukotriene A4 synthetase activity. Leukotriene A4, an unstable epoxide, is hydrolyzed to leukotriene B4 or conjugated with glutathione to yield leukotriene C4 and its metabolites, leukotriene D4 and leukotriene E4. The leukotrienes participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. Recent studies also suggest a neuroendocrine role for leukotriene C4 in luteinizing hormone secretion. Lipoxins are formed by the action of 5- and 15-lipoxygenases on arachidonic acid. Lipoxin A causes contraction of guinea pig lung strips and dilation of the microvasculature. Both lipoxin A and B inhibit natural killer cell cytotoxicity. Thus, the multiple interaction of lipoxygenases generates compounds that can regulate specific cellular responses of importance in inflammation and immunity.

https://science.sciencemag.org/content/sci/237/4819/1171.full.pdf

Leukotrienes and lipoxins: structures, biosynthesis, and biological effects

Mammalian lipoxygenases: molecular structures and functions.

Recent developments in biochemistry of the plant lipoxygenase pathway.

Lipoxin biosynthesis and its impact in inflammatory and vascular events

Enzymology and physiology of reticulocyte lipoxygenase: comparison with other lipoxygenases.

https://febs.onlinelibrary.wiley.com/doi/epdf/10.1016/0014-5793%2886%2980752-9

H. Stender

Papers

Requirement of monohydroperoxy fatty acids for the oxygenation of 15LS-HETE by reticulocyte lipoxygenase.

Formation of lipoxin B by the pure reticulocyte lipoxygenase.

The formation of products containing a conjugated tetraenoic system by pure reticulocyte lipoxygenase