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Effects of the Prostaglandin Synthetase Inhibitor Indomethacin on Tumorigenesis, Tumor Proliferation, Cell Kinetics, and Receptor Contents of 7,12-Dimethylbenz(a)anthracene-induced Mammary Carcinoma in Sprague-Dawley Rats Fed a High- or Low-Fat Diet

Department of Surgery (II), School of Medicine, Kanazawa University [M. N., T. T., N. K., T. K., I. M.], and Operation Center [M. N.], Pathology Unit [Y. M.], Kanazawa University Hospital, Takara-machi, 13-1, Kanazawa 920, Japan

The effects of indomethacin on tumorigenesis, tumor proliferation, cell kinetics, and receptor content of 7,12-dimethylbenz(a)anthracene-induced mammary carcinoma have been examined in female Sprague-Dawley rats. The rats were fed either a high-fat (20% corn oil) or low-fat (0.5% corn oil) diet with or without 0.005% indomethacin starting 7 days after intragastric administration of a single dose of 5 mg 7,12-dimethylbenz(a)anthracene. The results demonstrated that indomethacin completely blocked the stimulatory effect of fat on tumorigenesis, as demonstrated by a decreased tumor incidence, a decreased number of tumors per group, and an increased latency. Contrary to what had been expected, however, indomethacin promoted tumor proliferation in both the high- and low-fat diet groups, as evidenced by an increased tumor size, an increased bromodeoxyuridine-labeling index, and a decreased potential tumor-doubling time. No significant difference in either the estrogen receptor or progesterone receptor content of the tumor was noted. It can be concluded, therefore, that indomethacin significantly reduced tumorigenesis in the high-fat diet group but significantly promoted tumor proliferation in both the high- and low-fat diet groups.

¹ To whom requests for reprints should be addressed, at The Operation Center, Kanazawa University Hospital, Takara-machi, 13-1, Kanazawa 920, Japan.

Received 4/ 3/90. Accepted 3/ 8/91.

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