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Long-Term Effects of Neonatal Hormonal Treatments on Plasma Prolactin Levels in Female BALB/cfC3H and BALB/c Mice

Pharmacology Division, National Cancer Center Research Institute, Tsukijl, Chuo-ku, Tokyo 104 Japan [H. N., R. Y.]; Zoological Institute, Faculty of Science, University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113, Japan [T. M.]; and Department of Zoology and Cancer Research Laboratory, University of California, Berkeley, California 94720 [H. A. B., K. T. M.]

In view of morphological indications that the effect of neonatal sex steroid exposure on mammary gland development and tumorigenesis in mice may be a consequence of sustained prolactin secretion, homologous radioimmunoassay was used to measure plasma prolactin levels in variously treated mice at several ages. Female BALB/cfC3H/Crgl and BALB/cCrgl mice received daily s.c. injections of 5 µg dithylstilbestrol, 20 µg diethylstilbestrol, 20 µg 17ß-estradiol, 20 µg testosterone, or 20 µg ovine prolactin for the first 5 days of postnatal life. In mice killed at about 2, 7, and 15 months of age, plasma prolactin levels of BALB/cfC3H females treated neonatally with diethylstilbestrol, 17ß-estradiol, or prolactin were comparable with those of the controls at proestrus/estrus and usually were significantly higher than the levels in those at metestrus/diestrus. Prolactin levels in mice treated with testosterone were usually significantly higher than were those in the other treated groups and in all control groups. In BALB/c females at about 7 and 15 months, most sterold-treated groups showed prolactin levels greater than control values at metestrus/diestrus but comparable with those at proestrus/estrus. However, testosterone treatment resulted in levels greater than those of controls at either stage. In both substrations mice given steroid hormones or diethylstilbestrol lacked ovarian corpora lutea at all ages, but control mice and mice receiving prolactin showed corpora lutea. Mammary gland responses to neonatal steroid or diethylstilbestrol treatment may in part be ascribed to continuous estrogen stimulation of prolactin secretion.

¹ Recipient of grants-in-aid from cancer research from the Ministry of Education, Science and Culture, Japan (No. 001043 and 001080) and of a Travel Fellowship, International Agency for Research on Cancer, World Health Organization, 1974 (T. 885).

² Recipients of U. S.-Japan Cooperative Science Program Grants NSF RF 39781 and JSPS SR055.

³ Recipient of NIH Grant CA-05388. To whom requests for reprints should be addressed.

Received 5/23/77. Accepted 1/11/78.

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