Fletcher-Cieutat M, Vanderhoek J Y, Bryant R W, Bailey J M
Prostaglandins Leukot Med. 1985 May;18(2):255-9. doi: 10.1016/0262-1746(85)90025-3.
Human platelets metabolize arachidonic acid via cyclooxygenase (E.C. 1.14.99.1) to thromboxane A2 and the 12-lipoxygenase to 12-hydroxyeicosatetraenoic acid (12-HETE). Aspirin inhibits cyclooxygenase while the neutrophil product 15-Hydroxyeicosatetraenoic acid (15-HETE) is a selective inhibitor of platelet 12-lipoxygenase. The unexpected observation was made that the platelet 12-lipoxygenase of individuals who had ingested aspirin showed up to a twenty-fold increase in sensitivity to inhibition by 15-HETE. This observation was confirmed in platelets treated with aspirin in vitro. Aspirin pretreatment consistently resulted in a decrease in the I50 for 15-HETE from an average of 21.5 microM to only 5.2 +/- 1.5 microM, indicating a probable interaction between the cyclooxygenase and lipoxygenase pathways.
人类血小板通过环氧合酶（E.C. 1.14.99.1）将花生四烯酸代谢为血栓素A2，并通过12-脂氧合酶将其代谢为12-羟基二十碳四烯酸（12-HETE）。阿司匹林抑制环氧合酶，而中性粒细胞产物15-羟基二十碳四烯酸（15-HETE）是血小板12-脂氧合酶的选择性抑制剂。有一个意外的发现，即摄入阿司匹林的个体的血小板12-脂氧合酶对15-HETE抑制的敏感性提高了多达20倍。这一发现在用阿司匹林体外处理的血小板中得到了证实。阿司匹林预处理始终导致15-HETE的半数抑制浓度（I50）从平均21.5微摩尔降至仅5.2±1.5微摩尔，表明环氧合酶和脂氧合酶途径之间可能存在相互作用。
