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SUMMARY
Four-day cyclic rats fed 7,12-dimethylbenz(a)anthracene (DMBA) (20 mg) at 50 days of age had peak prolactin, oestradiol and uterine wet weights at pro-oestrus. Tamoxifen (50, 200 and 800 μg daily), administered to ovariectomized rats, produced significant (P < 0·05) decreases in oestrogen-stimulated prolactin levels but was unable to reduce prolactin to control values. Tamoxifen (12·5, 50 and 200 μg daily) produced decreases in size in DMBAinduced rat mammary carcinomata in intact rats although some tumours did not respond to therapy. The ability of the pituitary to produce prolactin was not impaired. Decreases in uterine wet weights and peripheral oestradiol levels occurred during tamoxifen treatment.
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Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545, U.S.A.
(Received 28 August 1974)
Harper & Walpole (1967 reported the potent antioestrogenic activity of ICI 46,474, the trans-isomer of 1-(p-β-dimethylaminoethoxyphenyl)-1,2-diphenylbut-1-ene, in the rat; however, in the mouse the compound exhibited only oestrogenic properties. However, Emmens (1971) showed that large doses of ICI 46,474 or the related compound H774 (1-(p-β-diethylaminoethoxyphenyl)-1,2-di(p-methoxyphenyl)-but-1-ene citrate) caused vaginal refractoriness to oestradiol for several weeks after s.c. administration to ovariectomized mice. The present study was undertaken to determine the ability of ICI 46,474 and H774 to inhibit binding of [3H]oestradiol to the 8 S oestrogen receptor derived from ovariectomized mouse uterus and vagina.
Mature, Charges River CD strain mice were ovariectomized under ether anaesthesia, primed with 1 μg oestradiol-17β in 0·05 ml peanut oil and used for experimentation 2 weeks later. Animals were killed by cervical dislocation and the uteri and vaginae were dissected out, weighed and immediately
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Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545, U.S.A.
(Received 8 November 1974)
Oestrogens have been found to stimulate prolactin release in the rat (Chen & Meites, 1970) and increases in prolactin in the circulation have been reported to be essential for the maintenance and growth of dimethylbenz(α)anthracene (DMBA)-induced rat mammary carcinomata (Pearson, Molina, Butler, Llerena & Nasr, 1972). Non-steroidal anti-oestrogens retard the growth of DMBA-induced rat mammary carcinoma (Schulz, Haselmayer & Hölzel, 1971; Terenius, 1971) and one such compound nafoxidine (U-11, 100A) has been shown to inhibit oestrogen-stimulated prolactin release in rats (Heuson, Waelbroeck, Legros, Gallez, Robyn & L'Hermite, 1971–72) thereby suggesting a mechanism for antitumour activity which may occur simultaneously with tumour oestrogen receptor blockade (Terenius, 1971). The present investigation was undertaken to determine whether other anti-oestrogens could control oestrogen-stimulated prolactin release.
The non-steroidal anti-oestrogens ICI 46,474 (tamoxifen, trade name Nolvadex, trans 1-(ρ-β-dimethylaminoethoxyphenyl)-1,2-diphenyl but-1-ene) and MER 25 (ethamoxytriphetol,
