Watanabe A, Yamauchi Y, Kobayashi M, Nagashima H
First Department of Internal Medicine, Okayama University Medical School, Japan.
Carcinogenesis. 1987 Oct;8(10):1445-8. doi: 10.1093/carcin/8.10.1445.
The potentiating effect of pre-existing cirrhosis on the formation of hyperplastic liver nodules and/or foci was investigated by feeding a low dose (0.008%) of 2-N-fluorenylacetamide (FAA) in a choline-deficient (CD) diet for 32 weeks to cirrhotic and non-cirrhotic rats. Liver cirrhosis was induced by feeding the rats a CD diet for the preceding 36 weeks. The number and area of gamma-glutamyltranspeptidase-positive hyperplastic liver nodules and/or foci were significantly larger in cirrhotic rats exposed to low-dose FAA than in non-cirrhotic rats similarly treated. Hyperplastic liver nodules and/or foci were not observed in rats continuously fed a CD diet alone for 68 weeks (control cirrhotic rats). The results suggest that cirrhotic liver might alter the metabolic response to FAA, even at low doses, and lead to enhanced induction of hyperplastic liver nodules and/or foci.
通过在胆碱缺乏(CD)饮食中给肝硬化和非肝硬化大鼠喂食低剂量(0.008%)的2-N-芴基乙酰胺(FAA)32周,研究了预先存在的肝硬化对增生性肝结节和/或病灶形成的增强作用。在之前的36周,给大鼠喂食CD饮食以诱导肝硬化。暴露于低剂量FAA的肝硬化大鼠中,γ-谷氨酰转肽酶阳性增生性肝结节和/或病灶的数量和面积显著大于同样处理的非肝硬化大鼠。连续68周单独喂食CD饮食的大鼠(对照肝硬化大鼠)未观察到增生性肝结节和/或病灶。结果表明,肝硬化肝脏可能会改变对FAA的代谢反应,即使在低剂量下,也会导致增生性肝结节和/或病灶的诱导增强。