Kitahashi Tsukasa, Tsujiuchi Toshifumi, Satoh Kenji, Ohtsuki Kozo, Konishi Yoichi, Tsutsumi Masahiro
Department of Food Science and Nutritional Health, Kyoto Prefectural University, Shimogamo, Kyoto 606-8522, Japan.
Exp Toxicol Pathol. 2004 Dec;56(3):153-7. doi: 10.1016/j.etp.2004.08.001.
Aberrant transcription of the fragile histidine triad (FHIT) gene was investigated in intrahepatic cholangiocellular carcinomas (ICCs) induced by N-nitrosobis(2-oxopropyl)amine (BOP) in female Syrian golden hamsters. The animals received 70 mg/kg of BOP followed by repeated exposure to an augmentation pressure regimen consisting of a choline-deficient diet combined with DL-ethionine and then L-methionine and administration of 20 mg/kg BOP. A total of 14 ICCs were obtained 10 weeks after the beginning of the experiment and total RNAs were extracted from each for assessment of aberrant transcription of the FHIT gene by reverse transcription-polymerase chain reaction analysis. Aberrant transcripts were detected in four out of 14 ICCs (28.6%), as absence in the regions of nucleotides (nt) -75 to 279, nt -75 to 348 and nt -75 to 447. These results suggest that alteration of the FHIT gene may play a role in a small fraction of ICCs induced by BOP in the hamster.
在雌性叙利亚金黄地鼠中，研究了由N-亚硝基双（2-氧代丙基）胺（BOP）诱导的肝内胆管细胞癌（ICC）中脆性组氨酸三联体（FHIT）基因的异常转录。动物接受70mg/kg的BOP，随后反复暴露于由胆碱缺乏饮食与DL-乙硫氨酸、然后L-甲硫氨酸联合组成的强化压力方案，并给予20mg/kg的BOP。实验开始10周后，共获得14个ICC，并从每个样本中提取总RNA，通过逆转录-聚合酶链反应分析评估FHIT基因的异常转录。在14个ICC中的4个（28.6%）检测到异常转录本，表现为核苷酸（nt）-75至279、nt -75至348和nt -75至447区域缺失。这些结果表明，FHIT基因的改变可能在仓鼠中由BOP诱导的一小部分ICC中起作用。
