Samuelsson B, Dahlén S E, Lindgren J A, Rouzer C A, Serhan C N
Science. 1987 Sep 4;237(4819):1171-6. doi: 10.1126/science.2820055.
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.
在细胞受到刺激时（例如，通过免疫复合物和钙离子载体），花生四烯酸从膜磷脂中释放出来，并通过一种同时具有白三烯A4合成酶活性的5-脂氧合酶转化为白三烯。白三烯A4是一种不稳定的环氧化物，可水解为白三烯B4或与谷胱甘肽结合生成白三烯C4及其代谢产物白三烯D4和白三烯E4。白三烯参与宿主防御反应和病理生理状况，如速发型超敏反应和炎症。最近的研究还表明白三烯C4在促黄体生成素分泌中具有神经内分泌作用。脂氧素是由5-脂氧合酶和15-脂氧合酶作用于花生四烯酸形成的。脂氧素A可引起豚鼠肺条收缩和微血管扩张。脂氧素A和B都能抑制自然杀伤细胞的细胞毒性。因此，脂氧合酶的多种相互作用产生了能够调节炎症和免疫中重要的特定细胞反应的化合物。
