Abe I, Sato S
Gan. 1976 Feb;67(1):55-65.
Change in beta-glucuronidase activity of six Yoshida ascites hepatomas was examined after treatment of host rats with one of 12 anticancer agents. The hepatomas, AH-66F, AH-130, AH-109A, AH-60C, and AH-44, in decreasing order showed more or less distinct increase in beta-glucuronidase activity after treatment of the rats with Nitromin, Endoxan, 864-T, Carbazilquinone, Mitomycin-C, Toyomycin, Daunomycin, Neocarzinostatin, vincristine sulfate, 5-fluorouracil, or cytosine arabinoside only when the cytological effect was positive. Moreover, degree of the increase was generally correlated with that of cytological effect. Bleomycin was ineffective either enzymically or cytologically. AH-66 was insensitive to any of the agents tested in increasing beta-glucuronidase activity and showed only a very slight cytological response to some of the agents. Acid deoxyribonuclease behaved like beta-glucuronidase but to a lesser extent. The above order of drug sensitivity of the hepatomas was not in parallel with that of normal beta-glucuronidase level, which also did not correlate with the life span of host rats.
用12种抗癌药物之一处理宿主大鼠后,检测了6种吉田腹水肝癌的β-葡萄糖醛酸酶活性变化。在用氮芥、环磷酰胺、864-T、卡巴醌、丝裂霉素C、东洋霉素、柔红霉素、新制癌菌素、硫酸长春新碱、5-氟尿嘧啶或阿糖胞苷处理大鼠后,AH-66F、AH-130、AH-109A、AH-60C和AH-44这几种肝癌,按降序排列,仅在细胞学效应为阳性时,β-葡萄糖醛酸酶活性或多或少有明显增加。此外,增加的程度通常与细胞学效应的程度相关。博来霉素在酶学或细胞学方面均无效。AH-66对所测试的任何药物增加β-葡萄糖醛酸酶活性均不敏感,仅对某些药物表现出非常轻微的细胞学反应。酸性脱氧核糖核酸酶的表现与β-葡萄糖醛酸酶相似,但程度较轻。上述肝癌的药物敏感性顺序与正常β-葡萄糖醛酸酶水平的顺序不平行,正常β-葡萄糖醛酸酶水平也与宿主大鼠的寿命无关。