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Inhibition of Rat Mammary Carcinogenesis by Short Dietary Exposure to Retinyl Acetate¹

Institute of Environmental Medicine, New York University Medical Center, New York, New York 10016

Previous work has indicated that prolonged exposure to retinyl acetate in the diet can inhibit mammary cancers in rats given the carcinogen 7,12-dimethylbenz(a)anthracene. This study was designed to determine whether retinyl acetate was an effective inhibitor when given for short periods at the time of and after the administration of the carcinogen. Virgin female Lewis rats were given 20 mg 7,12-dimethylbenz(a)anthracene in 1 ml sesame oil intragastrically at 50 days of age. The rats were fed Purina laboratory chow supplemented with 250 ppm retinyl acetate in groups of 20 according to the following schedule: -2 to +1 weeks; +1 to +30 weeks; +1 to +12 weeks; +12 to +30 weeks; -2 to +30 weeks; and none, where Time 0 was the day of 7,12-dimethylbenz(a)anthracene administration. Otherwise, animals were given standard Purina laboratory chow. At 30 weeks, groups receiving retinyl acetate from -2 to +1, +1 to +30, +12 to +30, and -2 to +30 all showed a significant decrease in tumor multiplicity in comparison to non-retinyl acetate-treated controls. The greatest decrease was seen in the longest treatment group (-2 to +30 weeks), but a nearly equal reduction was seen in the group receiving a short retinyl acetate exposure at the time of carcinogen availability (-2 to +1 weeks). In the +1 to +12 group, the inhibition of tumor development was temporary, inasmuch as tumor values returned to control levels by Week 30. These results indicate that retinyl acetate inhibition of mammary cancer is not limited to the late stage of the disease, because the retinoid was almost equally effective when given for a short period at the time of carcinogen availability.

¹ This work was supported by United States Department of Energy Contract EY-76-S-02-2737 and National Institute of Environmental Health Sciences Grant ES-00260. Presented in part at the Annual Meeting of the American Association for Cancer Research, New Orleans, La., May, 1979 (11).

² Performed in partial fulfillment of the requirements for a Ph.D. in the collaborative program in Environmental Medicine and Biology, Graduate School of Arts and Sciences, New York University. Present address: Life Sciences Division, IIT Research Institute, 10 West 35th Street, Chicago, Ill. 60616.

³ To whom requests for reprints should be addressed, at Institute of Environmental Medicine, New York University Medical Center, 550 First Avenue, New York, N. Y. 10016.

Received 10/26/79. Accepted 12/27/79.

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