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[Cancer Research 49, 3287-3289, June 15, 1989]
© 1989 American Association for Cancer Research

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Inhibition of Methylnitrosourea-induced Large Bowel Cancer Development in Rats by Sarcophytol A, a Product from a Marine Soft Coral Sarcophyton glaucum1

Tomio Narisawa2, Masahiro Takahashi, Makoto Niwa, Yoko Fukaura and Hirota Fujiki

Department of Surgery, Akita University School of Medicine, Akita 010 [T. N., M. T., M. N., Y. F.], and Cancer Prevention Division, National Cancer Center Research Institute, Chuo-ku, Tokyo 104 [H. F.], Japan

An antitumorigenic effect of sarcophytol A (SaA), a simple monohydroxycembratetraene isolated from a marine soft coral Sarcophyton glaucum, was investigated in rat colon carcinogenesis. Three groups (26 rats each) of female CD-Fischer rats given an intrarectal dose of 2 mg of N-methyl-N-nitrosourea 3 times weekly for Wk 1 to 3 were fed standard laboratory chow in the control group or the chow containing 0.01% SaA from Wk 1 or from Wk 4 in experimental groups. The body weight gain and the food intake were not different among all 3 groups, and SaA intake was similar in both experimental groups at a dosage of 6.18 and 6.14 mg/kg of body weight/day at Wk 5 and 3.87 and 3.90 mg/kg of body weight/day at Wk 25. At autopsy at Wk 26, the incidence of large bowel tumors was found to be significantly lower and the mean number of tumors per tumor-bearing rat to be insignificantly smaller in experimental groups than in the control group: 50% and 58% versus 85%, 1.8 and 1.8 versus 2.0. The tumors in both experimental groups were generally smaller. All the tumors except two signet ring cell carcinomas were well-differentiated adenocarcinomas. Induction of ornithine decarboxylase activity, a marker of tumor promotion, in the large bowel mucosa of rats which were fed the SaA chow for 1 wk, then received an intrarectal dose of 12, 6, or 1.2 µmol of deoxycholate, a tumor promoter in large bowel carcinogenesis, and were killed 4 h later was significantly lower than in control rats. Thus, it was concluded that SaA inhibited the development of large bowel cancer, probably through an antipromoting mechanism.

1 Supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Health and Welfare, Japan.

2 To whom requests for reprints should be addressed.

Received 10/21/88. Revised 3/13/89. Accepted 3/21/89.




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Copyright © 1989 by the American Association for Cancer Research.