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本文证明DENA诱发的大鼠肝癌结节中维生素K依赖性羧化酶活性显著降低,外源多肽羧化酶活性只有正常大鼠肝脏中的62.6％,而内源蛋白质前体羧化酶活性仅为27％。华法令能在正常大鼠肝脏中诱导羧化酶的合成,而这种诱导能力在诱癌晚期的肝癌大鼠肝脏中明显下降。上述结果说明肝癌细胞中维生素K依赖性羧化酶的合成受阻,造成肝癌组织中羧化酶的缺乏。诱癌过程中大鼠肝脏维生素K依赖性羧化酶活性和血浆异常凝血酶原水平形成良好的对应关系。随着肝癌组织的增大,肝癌细胞分泌入血的异常凝血酶原水平显著升高,诱癌第20周时的大鼠血浆中异常凝血酶原含量为正常大鼠的2.5倍。由此认为,肝癌组织由于不能合成足量的维生素K依赖性羧化酶,导致凝血酶原在成熟过程中羧化受阻,分泌入血形成高水平的异常凝血酶原。
This study demonstrated that DENA-induced rat liver cancer nodules in vitamin K-dependent carboxylase activity was significantly reduced, exogenous peptide carboxylase activity in normal rat liver only 62.6%, while the endogenous protein precursor carboxylase activity only 27%. Warfarin induces carboxylase synthesis in normal rat livers, and this induction is significantly reduced in the livers of late-stage liver cancer-bearing rats. The above results suggest that the synthesis of vitamin K-dependent carboxylase in HCC cells is blocked, resulting in a lack of carboxylase in HCC tissues. There is a good correspondence between the vitamin K-dependent carboxylase activity of rat liver and the level of plasma prothrombin in inducing cancer. With the increase of liver cancer tissues, the level of abnormal prothrombin released into the blood by hepatoma cells increased significantly. The content of abnormal prothrombin in rat plasma at the 20th week of cancer induction was 2.5 times of normal rats. Therefore, the liver cancer tissue can not synthesize enough vitamin K-dependent carboxylase, resulting in prothrombin in the process of carboxylation blocked, secreted into the blood to form a high level of abnormal prothrombin.