摘要
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。
During hepatocarcinogenesis induced by diethylnitrosamine (DENA) in rats, a period of decreased vitamin K-dependent carboxylase activity was observed followed by an increased period. Carfboxylase activity wat still lower in hepatoma nodules at the 20th week.As a result of reduced carboxylase activity, underoarboxylated prothrombin precursor accumulated greatly in the hepatoma nodules, with concomitant high concentrations of carboxylated precursor.Thus, the dynamics of abnormal plasma prothrombin showed a saddle-like curve consistent with the development of vitamin K-dependent carboxylase. It might be suggested that the increase of abnormal plasma prothrombin during hepatocaroinogenesis was mainly due to deficiency of vitamin K-dependent oarboxylase in tumor tissue, the deficiency of vitamin K being only a minor factor.
出处
《上海医科大学学报》
CSCD
1991年第4期269-273,共5页
Journal of Fudan University(Medical Science)
基金
国家自然科学基金资助课题(第386092号)
关键词
羧化酶
维生素K
异常凝血酶原
carboxylase
vitamin K
abnormal prothrombin
prothrombin precursor
hepatocellular carcinoma