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一、异常凝血酶原的来源和理化特性:正常凝血酶原是一种由肝内合成的维生素K 依赖性凝血因子,其氨基未端有10个羧化的谷氨酸残基。当维生素K 缺乏或摄入维生素K 拮抗剂时,肝细胞微粒体内维生素K 依赖性羧化酶的活力下降,导致谷氨酸羧化障碍或羧化不全,从而形成异常凝血酶原(DCP)。晚近,人们发现PHC 时DCP 升高,其因并非维生素K 缺乏所致,而是肝癌细胞自身具有合成和释放DCP 的功能。推测肝癌细胞中的维生素K 依赖性羧化体系功能存在障碍。
First, the source of abnormal prothrombin and physicochemical properties: Normal prothrombin is synthesized by the liver vitamin K-dependent coagulation factor, the amino end of 10 carboxylated glutamic acid residues. When vitamin K deficiency or vitamin K antagonist intake, vitamin K-dependent carboxylase activity in liver cell microsomal decreased, resulting in glutamate carboxylation or carboxylation, resulting in abnormal prothrombin (DCP). Recently, people found that DCC increased PHC, which is not due to vitamin K deficiency caused, but the liver cancer cells have their own synthesis and release of DCP function. It is speculated that there is a barrier to the function of vitamin K-dependent carboxylation system in liver cancer cells.