Effects of multiple pituitary homografts or progesterone on 7,12-dimethylbenz[a]anthracene-induced mammary tumors in rats.
Effects of multiple pituitary homografts or progesterone on 7,12-dimethylbenz[a]anthracene-induced mammary tumors in rats.
复制标题
多个垂体同种移植物或黄体酮对 7,12-二甲基苯并[a]蒽诱导的大鼠乳腺肿瘤的影响。
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发表时间:
1968
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影响因子:
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通讯作者:
J. Meites
中科院分区:
文献类型:
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作者:
C. Welsch;J. Clemens;J. Meites
This investigation evaluates the effects of prolactin-secreting pituitary homografts and progesterone on the induction of mamary tumors in female rats subsequently treated with 712-dimethylbenz[alpha]anthracene (DMBA). Immature female Sprague-Dawley rats were divided into 5 groups: group 1 intact controls; group 2 ovariectomized; group 3 intact and 4 pituitary homografts; group 4 ovariectomized and 4 pituitary homografts; and group 5 intact and given injection of 4 mg progesterone daily. Pituitary transplantation and/or ovariectomy were performed at age 25 days. Progesterone was injected beginning at 30 days of age and continued for 40 consecutive days. At age 55 days all animals were given a single intravenous dose of 5 mg DMBA. At the end of the study the percent of tumor incidence average number of tumors/rat and average total weight of tumors/rat (g) were: group 1 100% 12.2 +or- 1.2 16.2 +or- 3.5; group 2 0; group 3 73% 4.7 +or- 1.3 5.4 +or- 2.0; group 4 0; and group 5 79% 3.3 +or- 0.7 5.9 +or- 4.6. Percentage of rats with tumors average number of tumors/rat and average total weight of tumors/rat were significantly decreased in intact rats bearing 4 pituitary homografts and in intact rats given injections of progesterone as compared to the intact controls. The inhibitory effect of the prolactin-secreting pituitary homografts appears to be mediated at least in part through the ovary since daily injections of progesterone resulted in a comparable inhibition of mammary tumorigenesis. These data indicate that prolactin and/or progesterone by stimulating growth and development growth of the mammary gland inhibit DMBA-induced mammary tumorigenesis if given sufficiently prior to carcinogen treatment. (authors)