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Influence of Dietary Fat and Indomethacin on the Growth of Transplantable Mammary Tumors in Rats¹

Cancer Research Program, Oklahoma Medical Research Foundation [G. M. K., C. D.], Biomembrane Research Laboratory, Oklahoma Medical Research Foundation [M. M. K.], and Department of Pathology, Oklahoma University Health Sciences Center [S. D. K.], Oklahoma City, Oklahoma 73104

Studies were designed to determine if treatment with indomethacin influenced the growth of a transplantable, metastatic, rat mammary tumor. Female, Wistar-Furth inbred rats were fed either a standard chow diet or a semipurified diet containing 2, 5, 10, or 20% stripped com oil. Indomethacin was given in drinking water, and rats consumed between 2.5 and 3.0 mg indomethacin/kg body weight/day. Feeding of diets and initiation of treatment with indomethacin were started when rats were weaned (21 days old) and continued until they were killed. Approximately 5 x 10³ mammary tumor cells (DMBA-4) were injected into the fat pad of the sixth mammary gland which is adjacent to the right inguinal lymph node. Each dietary/treatment group consisted of at least 10 rats. Since indomethacin inhibits prostaglandin synthesis, two other groups of non-tumor-bearing rats were used to determine if dietary fat and treatment with indomethacin either influenced prostaglandin E₂ production (in vitro) by mononuclear cells from the spleen or altered serum levels of fatty acids. Results indicated that: (a) the rate of tumor growth in untreated rats was significantly greater when the dietary fat content was either 10 or 20% compared to diets containing either 2 or 5% fat; (b) the tumor growth-promoting effects of 10 and 20% fat diets were completely abrograted in rats treated with indomethacin; (c) treatment with indomethacin also inhibited tumor growth in rats fed diets containing either 2 or 5% fat; (d) synthesis of prostaglandin E₂ by mononuclear cells from the spleens of untreated rats increased as the dietary fat content increased; (e) in indomethacin-treated rats, prostaglandin E₂ synthesis was inhibited in all dietary groups and was not dependent on dietary fat; and (f) in both untreated and indomethacin-treated rats, the serum concentrations of oleic and linoleic acids were influenced to the same extent by dietary fat.

¹ This investigation was supported by PHS Grant No. CA 33705 awarded by the National Cancer Institute, Department of Health and Human Services, and by NIH Grant No. ES01789.

Received 12/12/82. Accepted 7/13/83.