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Effect of Retinyl Acetate on the Occurrence of Ovarian Hormone-responsive and -nonresponsive Mammary Cancers in the Rat¹

Departments of Home Economics [H. J. T., A. R. T.] and Mathematics [L. D. M.], University of New Hampshire, Durham, New Hampshire 03824, and Food and Drug Research Laboratories, Inc., Waverly, New York 14892 [P. J. B.]

The inhibitory activity of retinyl acetate against the induction of ovarian hormone-responsive and -nonresponsive mammary gland adenocarcinomas was studied in intact and castrated female Sprague-Dawley rats. Three experiments were conducted. Mammary cancer was induced by a single p.o. administration of 7,12-dimethylbenz(a)anthracene (DMBA) at 50 days of age. Animals in Experiments 1 and 2 each received 20 mg DMBA, whereas those in Experiment 3 received 15 mg. In all experiments, animals were fed a chow diet supplemented per kg with either a placebo or 328 mg retinyl acetate starting 7 days after carcinogen treatment. In Experiment 1, rats were castrated at either 7, 60, or 90 days postcarcinogen and were killed 120 days after DMBA was given. In Experiment 2, rats were castrated 30 days after DMBA and were killed 240 days after carcinogen treatment. In Experiment 3, rats were castrated when a detected tumor attained a measurable diameter, and the hormone responsiveness of their tumors was subsequently determined. The experiment was terminated 279 days after DMBA treatment. In both intact and castrated rats, mammary tumor occurrence was inhibited by treatment with retinyl acetate. However, there were no differences in the latency to appearance time of hormone-responsive and -nonresponsive cancers in intact animals receiving either placebo or retinyl acetate. The data indicate that retinyl acetate inhibits DMBA-induced mammary tumorigenesis in either the presence or the absence of the ovaries. It appears that retinyl acetate is effective in inhibiting both ovarian hormone-responsive and -nonresponsive mammary tumors.

¹ Supported in part by Central University Research Fund. University of New Hampshire; by New Hampshire Agricultural Experiment Station Project 251; by Food and Drug Research Laboratories, Inc.; and by Grant CA 28109 from the National Cancer Institute. Scientific Contribution 1034 from the New Hampshire Agricultural Experiment Station.

² To whom requests for reprints should be addressed at Department of Home Economics, Pettee Hall, University of New Hampshire, Durham, N. H. 03824.

Received 6/ 2/80. Accepted 12/ 1/81.