Nakae D, Yoshiji H, Maruyama H, Kinugasa T, Denda A, Konishi Y
Department of Oncological Pathology, Nara Medical University.
Jpn J Cancer Res. 1990 Nov;81(11):1081-4. doi: 10.1111/j.1349-7006.1990.tb02515.x.
The comparative carcinogenic activities of a choline-deficient, L-amino acid-defined diet (CDAADD) and a purified choline-deficient diet (CDD) for rat liver were studied in terms of both 8-hydroxydeoxyguanosine induction, a marker of DNA damage induced by oxidative stress, and development of gamma-glutamyltransferase (GGT)-positive putative preneoplastic lesions, including foci and hyperplastic nodules. Twelve weeks after the beginning of treatment, DNA damage could be detected in the liver DNA of rats receiving either CDAADD or CDD, the degree being significantly greater in the former case. Similarly, while GGT-positive liver lesions were induced by both CDAADD and CDD, the numbers were higher and the areas of lesions were larger in rats receiving CDAADD than in those given CDD. Histologically, hyperplastic nodules were induced in the livers of animals administered CDAADD whereas only foci were seen in the CDD case. The results thus indicate that oxidative stress might be directly involved in rat liver carcinogenesis by CDD and, to a greater degree, with CDAADD.
通过8-羟基脱氧鸟苷诱导（氧化应激诱导的DNA损伤标志物）以及γ-谷氨酰转移酶（GGT）阳性的假定癌前病变（包括灶性病变和增生性结节）的发展，研究了胆碱缺乏、L-氨基酸限定饮食（CDAADD）和纯化的胆碱缺乏饮食（CDD）对大鼠肝脏的比较致癌活性。治疗开始12周后，在接受CDAADD或CDD的大鼠肝脏DNA中均可检测到DNA损伤，前者的损伤程度明显更大。同样，虽然CDAADD和CDD均可诱导GGT阳性肝脏病变，但接受CDAADD的大鼠病变数量更多，病变面积更大。组织学上，给予CDAADD的动物肝脏中诱导出增生性结节，而在给予CDD的情况下仅见灶性病变。因此，结果表明氧化应激可能直接参与CDD诱导的大鼠肝癌发生，在更大程度上也参与CDAADD诱导的大鼠肝癌发生。
