Mohan L C, Grantham P H, Weisburger E K, Weisburger J H, Idoine J B
J Natl Cancer Inst. 1976 Apr;56(4):763-8. doi: 10.1093/jnci/56.4.763.
The metabolism of N-2-fluorenylacetamide (FAA) and N-hydroxy-2-fluorenylacetamide (N-OH-FAA) was studied in groups of rats that had been prefed the protective agent p-hydroxyacetanilide (p-OH-AA) alone or in combination with each of the carcinogens for 4 weeks. Compared with controls, pretreatment increased the percentage of metabolites in the urine, chiefly as glucuronic acid conjugates, whereas the fecal excretion of FAA metabolites was lowered. The levels of total and tissue-bound material in the liver and blood plasma were also lower after prefeeding. Liver aryl hydrocarbon hydroxylase and liver deacetylase were not affected by p-OH-AA pretreatment. However, liver glucuronyl transferase was increased by either prefeeding with p-OH-AA and/or the carcinogen. The protective effect of p-OH-AA against liver tumor induction with FAA or N-OH-FAA may in part result from a combination of the decreased binding of carcinogen to hepatic cellular macromolecules and the increased excretion as the glucuronide conjugates.
在预先单独喂食保护剂对羟基乙酰苯胺（p - OH - AA）或与每种致癌物联合喂食4周的大鼠组中，研究了N - 2 - 芴基乙酰胺（FAA）和N - 羟基 - 2 - 芴基乙酰胺（N - OH - FAA）的代谢情况。与对照组相比，预处理增加了尿液中代谢物的百分比，主要是以葡萄糖醛酸结合物的形式，而FAA代谢物的粪便排泄量降低。预先喂食后，肝脏和血浆中总物质及组织结合物质的水平也较低。肝脏芳烃羟化酶和肝脏脱乙酰酶不受p - OH - AA预处理的影响。然而，单独预先喂食p - OH - AA和/或致癌物均可增加肝脏葡萄糖醛酸转移酶。p - OH - AA对FAA或N - OH - FAA诱导肝脏肿瘤的保护作用可能部分源于致癌物与肝细胞大分子结合减少以及葡萄糖醛酸结合物排泄增加的共同作用。
