Yahn D M, Feinstein M B
Prostaglandins. 1981 Feb;21(2):243-54. doi: 10.1016/0090-6980(81)90141-6.
L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK) was found to inhibit several aspects of arachidonic acid (20:4) metabolism in human platelets; the primary effect being inhibition of thromboxane synthetase. Thromboxane B2 (TxB2) formation from exogenous 20:4 or PGH2, or from endogenous 20:4, was inhibited by TPCK at concentrations between 0.1 and 0.5 mM. Formation of malondialdehyde (MDA) and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT), products which also arise from PGH2, was inhibited to a similar extent. Inhibition of formation from 20:4 of 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE), the product of the lipoxygenase pathway, was observed; although the extent of this inhibition was less than that of TxB2 formation. A small inhibitory effect of TPCK on the release of 20:4 from platelet phospholipids was also observed. This evidence indicated that while a number of reactions are inhibited by TPCK, the primary effect appears to be inhibition of thromboxane synthetase.
已发现L-1-对甲苯磺酰胺基-2-苯乙基氯甲基酮（TPCK）可抑制人血小板中花生四烯酸（20:4）代谢的多个方面；主要作用是抑制血栓素合成酶。在0.1至0.5 mM的浓度下，TPCK可抑制外源性20:4或PGH2，或内源性20:4生成血栓素B2（TxB2）。丙二醛（MDA）和12-L-羟基-5,8,10-十七碳三烯酸（HHT）（同样由PGH2生成的产物）的生成也受到类似程度的抑制。观察到TPCK抑制花生四烯酸通过脂氧合酶途径生成12-L-羟基-5,8,10,14-二十碳四烯酸（HETE）；尽管这种抑制程度小于TxB2的生成。还观察到TPCK对血小板磷脂释放20:4有轻微抑制作用。这一证据表明，虽然TPCK可抑制多种反应，但其主要作用似乎是抑制血栓素合成酶。
