在二乙基亚硝胺(DENA)诱发大鼠肝癌过程中,维生素K依赖性羧化酶活性呈现先降低、后升高的现象。在诱癌第20周的肝癌结节中羧化酶活性很低。未羧化凝血酶原前体在肝癌结节中大量堆积,已羧化凝血酶原前体也有类似的堆积现象。诱癌过程中血浆异常凝血酶原呈现马鞍形的变化,这与羧化酶的变化密切相关。癌变时血浆异常凝血酶原的升高主要是由于肝脏羧化酶的缺乏所致,维生素K的缺乏仅是次要因素。 In the process of diethylnitrosamine (DENA) -induced hepatocarcinogenesis, the activity of vitamin K-dependent carboxylase decreased first and then increased. In the first 20 weeks of cancer induced liver cancer nodules carboxylase activity is low. Uncarboxylated prothrombin precursors accumulate in large numbers in hepatic carcinoma nodules, and similar accumulation phenomena have been observed for carboxylated prothrombin precursors. Abnormal prothrombin in the process of carcinogenesis showed saddle-shaped changes, which is closely related to the changes of carboxylase. Malignant plasma abnormal prothrombin increased mainly due to the lack of liver carboxylase, vitamin K deficiency is only a secondary factor.