Willingham A K, Matschiner J T
Biochem J. 1974 Jun;140(3):435-41. doi: 10.1042/bj1400435.
The oxidation of phylloquinone to the 2,3-epoxide (by phylloquinone epoxidase) was studied in liver from control and warfarin-resistant rats. The reaction requires microsomal fraction, soluble protein, a heat-stable soluble factor and O(2). It is not inhibited by CO or CN(-). Epoxidase activity was stimulated if plasma prothrombin was lowered either by anticoagulants or the absence of vitamin K. The activity of the enzyme rapidly returned to normal values after the administration of vitamin K to hypoprothrombinaemic rats. These differences in the activity of the enzyme occur in the microsomal fraction and not the cytosol. A thrombin-generating polypeptide that accumulates in microsomal fraction of hypothrombinaemic rats correlated directly with epoxidase activity. These data support the view that enzymic interconversion of phylloquinone and its 2,3-epoxide participates in the biological activity of vitamin K.
在对照大鼠和对华法林耐药的大鼠肝脏中,研究了叶绿醌被(叶绿醌环氧化酶)氧化为2,3 - 环氧化物的过程。该反应需要微粒体部分、可溶性蛋白、一种热稳定的可溶性因子和氧气。它不受一氧化碳或氰离子抑制。如果通过抗凝剂或缺乏维生素K使血浆凝血酶原降低,环氧化酶活性会受到刺激。给低凝血酶原血症大鼠施用维生素K后,该酶的活性迅速恢复到正常值。这些酶活性的差异出现在微粒体部分而非胞质溶胶中。在低凝血酶原血症大鼠微粒体部分积累的一种凝血酶生成多肽与环氧化酶活性直接相关。这些数据支持这样一种观点,即叶绿醌及其2,3 - 环氧化物的酶促相互转化参与了维生素K的生物活性。