Ogawa K, Yokokawa K, Tomoyori T, Narasaki M
Int J Cancer. 1983 Jun 15;31(6):775-7. doi: 10.1002/ijc.2910310617.
Administration of ethylnitrosourea (ENU) to pregnant rats in the late stage of gestation has been known to have a mainly neurocarcinogenic action on the progeny. However, when transplacental administration of ENU was combined in postnatal life with a brief dietary exposure to 2-acetylaminofluorene (2-AAF) and a two-thirds partial hepatectomy, numerous focal hyperplastic lesions of gamma-glutamyltranspeptidase (GGT)-positive hepatocytes emerged in the liver of the progeny. On the other hand, rats of F2 generation born of F1 parents and F3 rats born of F2 parents showed no increase in the incidence of hepatic lesions after treatment with the same dietary regimen. It was suggested that direct interaction between fetal liver cells and the carcinogen is important for occurrence of initiated hepatocytes and that the initiation effect on rat liver by ENU does not persist in the descendants of F2 and F3 generations.
已知在妊娠后期给怀孕大鼠施用乙基亚硝基脲(ENU)对后代主要具有神经致癌作用。然而,当在出生后经胎盘施用ENU与短期饮食接触2-乙酰氨基芴(2-AAF)以及三分之二部分肝切除术相结合时,后代肝脏中出现了大量γ-谷氨酰转肽酶(GGT)阳性肝细胞的局灶性增生性病变。另一方面,由F1代亲本所生的F2代大鼠以及由F2代亲本所生的F3代大鼠在用相同饮食方案处理后,肝脏病变的发生率并未增加。这表明胎儿肝细胞与致癌物之间的直接相互作用对于起始肝细胞的发生很重要,并且ENU对大鼠肝脏的起始作用在F2和F3代的后代中不会持续存在。