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CARCINOGENICITY OF BRACKEN FERN IN ACI/N RATS
Kodama, Yukio,Sakai, Takeo,Yoon, Chong Sam,Horiuch, Shigetomo,Naito, Katsushi,Natori, Shisaku,Lee, Won Chang 대한보건협회 1990 대한보건연구 Vol.16 No.1
As part of a study to evaluate the caroinogenicity of bracken fern, we have prepared a freeze-dried extract of bracken fern(FDE-BF), spray-dried extract bracken fern(SDE-BF), or have used unprocessed bracken fern(UP-BF) and have mixed each with rat food and have fed these 3 separate diets to separate groups of rats(6 animals per group) for 27 weeks. After 27 weeks, all of these rats then were given basic diet without bracken fern or its extract and sacrificed after the 52nd week and examined. In group FDE-BF and SDE-BF, body weight gain were inhibited, and one rat in each of these two groups developed transitional cell carcinoma of urinary bladder. In group UP-BF, most rats died during the experimental period, and a transitional cell carcinoma, an adenocarcinoma of small intestine, and an adenocarcinoma of large intestine were observed in one rat and an adenocarcinoma of small intestine in each of 3 other rats of this group. Thus, the incidence of carcinoma was found to be markedly lower in Groups FDE-BF and SDE-BF than in Group UP-BF, indicating that the carcinogenicity of the unprocessed bracken fern to be more greater.
No Effect of High Fat Diet-Induced Obesity on Spontaneous Reporter Gene Mutations in gpt Delta Mice
Takasu, Shinji,Ishii, Yuji,Matsushita, Kohei,Kuroda, Ken,Kijima, Aki,Kodama, Yukio,Ogawa, Kumiko,Umemura, Takashi Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.17
A large number of epidemiological studies have demonstrated that obesity is a risk factor for several human cancers. Several animal studies using rodents with diet-induced or genetic obesity have also demonstrated that obesity can promote tumor development. However, the effects of obesity on the early stages of carcinogenesis, and especially on the spontaneous occurrence of somatic gene mutations, remain unclear. To investigate the effects of obesity on the rate of spontaneous gene mutations, we performed reporter gene mutation assays in liver, kidney, and colon, organs in which obesity appears to be associated with cancer development on the basis of epidemiological or animal studies, in mice with high fat diet (HFD)-induced obesity. Six-week-old male and female C57BL/6 gpt delta mice were fed HFD or standard diet (STD) for 13 or 26 weeks. At the end of the experiments, reporter gene mutation assays of liver, kidney, and colon were performed. Final body weights and serum leptin levels of male and female mice fed HFD for 13 or 26 weeks were significantly increased compared with corresponding STD-fed groups. Reporter gene mutation assays of liver, kidney, and colon revealed that there were no significant differences in gpt or $Spi^-$ mutant frequencies between STD- and HFD-fed mice in either the 13-week or 26-week groups. These results indicate that HFD treatment and consequent obesity does not appear to influence the spontaneous occurrence of somatic gene mutations.