论文部分内容阅读
分别测定二株不同生长率的肝癌细胞中氨基甲酰磷酸合成酶同工酶(CPSⅠ与CPSⅡ)的活性。结果:CPSⅠ与CPSⅡ活性均为正常肝大于实体肝癌细胞(H615肝癌),后者又大于腹水型肝癌细胞(H22)。提示CPSⅠ活性丧失的程度与肝癌的恶性程度相平行。恶性程度越高,CPSⅠ活性越低。CPSⅡ活性并不与肿瘤细胞的增殖率一致。从头合成途径可能不是肿瘤细胞中核苷酸合成的主要途径。
The activities of carbamyric synthase isoenzyme (CPSⅠand CPSⅡ) in two hepatocarcinoma cells with different growth rates were determined respectively. Results: The activity of CPSⅠ and CPSⅡ were both higher than that of HCC hepatocarcinoma (H615 hepatocarcinoma) and larger than that of ascites hepatoma cells (H22). Suggesting that the degree of loss of activity of CPS Ⅰ parallel with the degree of malignancy of liver cancer. The higher the degree of malignancy, the lower the activity of CPSI. CPSⅡ activity is not consistent with the proliferation rate of tumor cells. The de novo pathway may not be the primary pathway for nucleotide synthesis in tumor cells.