ANTI-OESTROGENIC EFFECTS OF NAFOXIDINE ON THE SYNTHESIS OF DNA BY THE RAT PITUITARY GLAND

1978 ◽  
Vol 76 (3) ◽  
pp. 555-556 ◽  
Author(s):  
J. M. JACOBI ◽  
H. M. LLOYD

Department of Medicine, University of Queensland, Clinical Sciences Building, Royal Brisbane Hospital, Queensland 4029, Australia Received 25 October 1977 One of the principal actions of oestrogens on their target organs is stimulation of the synthesis of DNA and cell division. In the rat pituitary gland, anti-oestrogens inhibit the oestrogen-induced increase in weight (Schreiber, Přibyl & Roháčová, 1972) and prevent the rise in the level of serum prolactin induced by oestradiol-17β (Jordan, Koerner & Robinson, 1975). The effects of anti-oestrogens on the synthesis of DNA by the pituitary gland have not been described. The experiments reported here show that the anti-oestrogen nafoxidine completely inhibits the synthesis of DNA and affects the secretion of growth hormone (GH) and prolactin in the male rat. Male Sprague–Dawley rats, 100 days old, were allowed free access to a pelleted diet and water and were maintained in a controlled environment (12 h light, 12 h darkness).

1977 ◽  
Vol 72 (1) ◽  
pp. 35-39 ◽  
Author(s):  
JOAN JACOBI ◽  
H. M. LLOYD ◽  
J. D. MEARES

SUMMARY The times of onset of oestrogen-induced prolactin secretion and DNA synthesis were studied in the pituitary gland of the male rat. At intervals from 3 to 96 h after injection of 10 mg diethylstilboestrol dipropionate, serum and pituitary prolactin concentrations were measured by radioimmunoassay and pituitary DNA synthesis by incorporation of [3H]thymidine in vitro. Serum prolactin was raised significantly from 6 h onwards and DNA synthesis was increased from 30 h onwards. Pituitary prolactin concentration began to increase at 30 h. Significant correlations were obtained between serum prolactin and DNA synthesis from 24 to 72 h but not during the period of prolactin secretion from 6 to 24 h.


1979 ◽  
Vol 82 (1) ◽  
pp. 131-133 ◽  
Author(s):  
REIKO YANAI ◽  
HIROSHI NAGASAWA

SUMMARY The effects of 2-hydroxyoestradiol-17β and 2-hydroxyoestriol (2OH-OE3) on levels of serum prolactin, DNA synthesis by the mammary gland and the weight of the uterus were examined in ovariectomized Sprague–Dawley rats. 2-Hydroxyoestradiol-17β had a potent oestrogenic activity in stimulating the secretion of prolactin by the pituitary gland, the synthesis of DNA by the mammary gland and in increasing the weight of the uterus. On the other hand, 2OH-OE3 increased the weight of the uterus only.


1964 ◽  
Vol 45 (4_Suppl) ◽  
pp. S139-S153 ◽  
Author(s):  
K. Junkmann ◽  
F. Neumann

ABSTRACT Experiments are described dealing with the mechanism of action of 6-chloro-Δ6-1,2α-methylene-17α-hydroxyprogesterone-acetate with regard to its anti-masculine effect on male rat foetuses, when administered to pregnant rats. It was shown that a marked direct anti-androgenic effect due to a competitive action on androgen receptors within the target organs, is probably the explanation of the mechanism of action. It was further shown that an oestrogenic effect or an appreciable inhibition of the pituitary gland respectively, can be ruled out as causative factors in the mechanism of action.


1984 ◽  
Vol 103 (3) ◽  
pp. 287-293 ◽  
Author(s):  
F. Di Carlo ◽  
S. Racca ◽  
G. Conti ◽  
E. Gallo ◽  
G. Muccioli ◽  
...  

ABSTRACT The changes in oestrogen, progesterone and prolactin receptor levels in target organs, and the macroscopic and microscopic modifications of uterus, ovary, adrenal and pituitary gland induced by long-term administration of high doses of medroxyprogesterone acetate (MPA) were investigated in female rats. Medroxyprogesterone acetate was injected i.m. for 30 days at daily doses of 7·5, 15 and 75 mg/kg. Oestrogen and/or progesterone-binding capacities were remarkably reduced at all doses of MPA used both in the uterus and pituitary gland. Furthermore, MPA caused a very evident reduction in the weight of pituitary glands, ovaries, adrenals and uterus. In all MPA-treated rats corpora lutea were absent from the ovaries, whereas the adrenals showed a significant reduction in the thickness of the cortex. In accordance with this, there was no evidence of ACTH-producing cells in the pituitary glands. Prolactin-producing cells were also absent, while GH-producing cells were present. Serum prolactin levels were significantly reduced at all doses of MPA used. A dramatic reduction of prolactin receptor concentrations was observed in the liver and the ovaries of MPA-treated rats. The results suggest that MPA acts as an antioestrogenic drug both by reducing the number of oestrogen receptors in target tissues and by changing the structure (and perhaps the function) of those organs (pituitary glands, ovaries and adrenals) which are, directly or indirectly, a source of oestrogens. The decreased synthesis of prolactin and the reduction of the number of prolactin receptors (which, on the contrary, are both increased by oestrogens) might be considered as additional antioestrogenic effects of MPA. J. Endocr. (1984) 103, 287–293


2009 ◽  
Vol 106 (3) ◽  
pp. 911-918 ◽  
Author(s):  
Zongjian Zhu ◽  
Weiqin Jiang ◽  
John N. McGinley ◽  
Henry J. Thompson

The objective of this experiment was to determine the effects on mammary carcinogenesis of similar limitations in energy availability either by energy expenditure due to moderate-intensity running (physical activity, PA) or by regulating dietary energy (RE) intake relative to a sedentary control (SC) group that ate ad libitum. A total of 90 female Sprague-Dawley rats were injected with 1-methyl-1-nitrosourea (50 mg/kg) and 7 days thereafter were randomized to either SC, a PA group given free access to a motorized running wheel, or a RE group whose food intake limited growth to the rate observed in PA. Compared with SC, mammary carcinogenesis was inhibited by RE or PA. Cancer incidence, 92.6%, 77.8%, and 66.7% ( P = 0.06), and cancer multiplicity, 3.44, 2.11, and 1.62 cancers/rat ( P = 0.006), in SC, RE, and PA, respectively, were reduced to a similar extent by RE and PA. Histological and Western blot analyses of mammary carcinomas provided evidence that RE and PA induced apoptosis via the mitochondrial pathway, that cell cycle progression was suppressed at the G1/S transition, and that intratumoral blood vessel density was reduced, although it remains to be determined whether PA and RE exert these effects via the same mechanisms.


1993 ◽  
Vol 5 (5) ◽  
pp. 553-556 ◽  
Author(s):  
Pablo-Manuel Dobado-Berrios ◽  
Songuyn Li ◽  
Ester Garcia Yebenes ◽  
Georges Pelletier

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