Suppr超能文献

在ICR/129Sv小鼠中,PARP-1缺陷不会增加4-硝基喹啉-1-氧化物(一种产生大分子加合物的致癌物)诱发的口腔和食管肿瘤的发生率。

Parp-1 deficiency does not increase the frequency of tumors in the oral cavity and esophagus of ICR/129Sv mice by 4-nitroquinoline 1-oxide, a carcinogen producing bulky adducts.

作者信息

Gunji Akemi, Uemura Akiko, Tsutsumi Masahiro, Nozaki Tadashige, Kusuoka Osamu, Omura Ken, Suzuki Hiroshi, Nakagama Hitoshi, Sugimura Takashi, Masutani Mitsuko

机构信息

Biochemistry Division, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.

出版信息

Cancer Lett. 2006 Sep 8;241(1):87-92. doi: 10.1016/j.canlet.2005.10.003. Epub 2005 Dec 9.

Abstract

The impact of poly(ADP-ribose) polymerase-1 (Parp-1)-deficiency on 4-nitroquinoline 1-oxide (4NQO)-induced carcinogenesis was studied in mice with an ICR/129Sv mixed genetic background. Parp-1(+/+), Parp-1(+/-) and Parp-1(-/-) animals given 4NQO for thirty-two weeks at 0.001% in their drinking water developed papillomas and squamous cell carcinomas of the tongue, palate and esophagus, but with no statistically significant variation with the Parp-1 genotype. Thus Parp-1 deficiency does not elevate susceptibility to carcinogenesis induced by a carcinogen which gives rise to bulky DNA lesions. This study also indicated that the ICR/129Sv mixed genetic background is associated with high yield induction of esophageal tumors by 4NQO.

摘要

在具有ICR/129Sv混合遗传背景的小鼠中,研究了聚(ADP-核糖)聚合酶-1(Parp-1)缺陷对4-硝基喹啉1-氧化物(4NQO)诱导致癌作用的影响。给Parp-1(+/+)、Parp-1(+/-)和Parp-1(-/-)的动物饮用含0.001% 4NQO的水32周,它们均出现了舌、腭和食管的乳头状瘤和鳞状细胞癌,但与Parp-1基因型无统计学上的显著差异。因此,Parp-1缺陷不会增加对导致大量DNA损伤的致癌物诱导致癌作用的易感性。该研究还表明,ICR/129Sv混合遗传背景与4NQO诱导食管肿瘤的高产率相关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验