The LOCALIZATION OF [6,7-3h]oestradiol-17β IN RAT UTERUS

King, R. J. B.; Gordon, Julius A.

doi:10.1677/joe.0.0340431

Cited by 55 publications

(14 citation statements)

References 10 publications

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“…In our in vivo experi ment, high levels of 3H-E2 were observed in the mammary tumors, uteri and vaginae. This also is consistent with the reports that the tumors, uteri and vaginae contain high levels of ER and are estrogen-target tissues (15,27). DROL and TAM significantly reduced the levels of 3H-E2 in the tumors and similarly re duced them in the uteri and vaginae in rats, suggesting that DROL has a high affinity to ER and that it inhibits the binding of E2 to ER in ER-positive mammary tumors.…”

Section: Discussionsupporting

confidence: 91%

Antitumor Effects of Droloxifene, a New Antiestrogen Drug, against 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors in Rats

Kawamura

Mizota²,

Kondo³

et al. 1991

Japanese Journal of Pharmacology

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ABSTRACT-The antitumor effects of droloxifene (DROL, (E)-a-[p-[2-(dimethyl amino)ethoxy]-phenyl]-a-ethyl-3-stilbenol), a new antiestrogen drug, on 7,12-dimethyl benz(a)anthracene (DMBA)-induced estrogen-dependent mammary tumors in rats were studied and compared with those of tamoxifen (TAM). Mammary tumors appeared from about 2 months after p.o. administration of DMBA to female rats, and all of them were estrogen receptor (ER) and progesterone receptor positive. DROL and TAM (p.o.) inhibited the growth of the tumors. Both drugs inhibited the binding of 125I-estradiol-17,9 to ER in the cytosol of the tumor in vitro, and the effect of DROL was much stronger than that of TAM. When 3H-estradiol-17(3 (3H-E2) was given s.c. to rats with the mammary tumors, 3H-E2 accumulated in the tumors, uteri and vaginae in which the ER levels are known to be high, but was low in the heart, in which the ER levels are normally low. DROL and TAM decreased the levels of 3H E2 in the tumors, uteri and vaginae, but had no effect in the hearts. When DROL or TAM was given p.o. to rats daily for 7 consecutive days after administration of DMBA, they inhibited the induction of mammary tumors by DMBA. From these re sults, DROL inhibits the growth and the initiation of DMBA-induced mammary tumors by inhibiting the binding of estrogen to its receptor.

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Section: Discussionsupporting

confidence: 91%

Antitumor Effects of Droloxifene, a New Antiestrogen Drug, against 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors in Rats

Kawamura

Mizota²,

Kondo³

et al. 1991

Japanese Journal of Pharmacology

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“…Ovariectomy of the rats was carried out under bromethol (Avertin, Winthrop Laboratories, New York) anaesthesia; the animals were used 6-7 days after the operation. Division of Chemistry and Biochemistry, Pathology Unit, and Electron Microscopy Unit, Imperial Cancer Research Fund, Lincoln's Inn Fields, London, W.C. 2 (Received 28 January 1966) Uterine epithelium was separated from muscle and stroma by gentle pressing between glass plates (King & Gordon, 1966).…”

Section: Animalsmentioning

confidence: 99%

“…181 picjpig.) has been described previously (King & Gordon, 1966). Each animal received a subcutaneous injection of [6,7-3H]-oestradiol (0-1 pig.¡100 g. body weight) in 0-9% (w/v) NaCl solution containing 10 % (v/v) ethanol.…”

Section: Animalsmentioning

confidence: 99%

The INTRANUCLEAR LOCALIZATION OF [6,7-3h]-Oestradiol-17β IN DIMETHYLBENZANTHRACENE-INDUCED RAT MAMMARY ADENOCARCINOMA AND OTHER TISSUES

King¹,

Gordon²,

Cowan³

et al. 1966

Journal of Endocrinology

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The intranuclear localization of [6,7-3H]oestradiol-17\g=b\(oestradiol) has been studied in nuclei from dimethylbenzanthracene (DMBA)-induced rat mammary adenocarcinoma, anterior pituitary, uterine epithelium and kidney. The evidence suggests that, with the possible exception of uterine epithelium, most of the oestrogen is associated with an acid-labile nonhistone component of the chromatin. No evidence has been found to suggest that oestradiol is associated with any particular type of chromatin. These results are compatible with the view that oestradiol affects cellular function in some tissues by altering the priming ability of the chromatin DNA.

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“…On the other hand, it is widely believed that the primary interaction of oestradiol in target organs is with a cytoplasmic receptor protein (Noteboom & Gorski, 1965;King & Gordon, 1966;Jensen, Suzuki, Kawashima, Stumpf, Jungblut & DeSombre, 1968). …”

Section: Introductionmentioning

confidence: 99%

MECHANISM OF OESTRADIOL ACTION ON THE RAT UTERUS: INDEPENDENCE OF CYCLIC AMP, PROSTAGLANDIN E2 AND Β-Adrenergic MEDIATION

Zor¹,

Koch²,

Lamprecht³

et al. 1973

Journal of Endocrinology

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The hypothesis that cyclic AMP plays an essential role in mediating the biological action of oestradiol on the uterus, was tested by determining the tissue concentration of the cyclic nucleotide after incubation of uteri of immature rats with oestradiol or after injection of this steroid into immature or ovariectomized rats. The effect of known stimulants of uterine adenyl cyclase, namely \g=b\-adrenergicdrugs and prostaglandin E2 (PGE2), on the level of cyclic AMP in the uterus was also examined both in vitro and in vivo.In either system, oestradiol failed to enhance the concentration of cyclic AMP in the uterine tissue, whereas adrenaline or the almost purely \ g = b \ \ x = r e q -\ adrenergic agonist isoprenaline (isoproterenol) caused cyclic AMP accumulation that was susceptible to inhibition by the \g=b\-adrenergicblocking agent propranolol. Prostaglandin E2, and to a much lesser degree prostaglandin F2\ g=a\ , increased cyclic AMP concentration in the uterus, but the effect of PGE2 was not inhibited by propranolol. It may be concluded that oestradiol does not cause appreciable stimulation of PGE2 synthesis or activation of \g=b\-adrenergicreceptors in the rat uterus since, otherwise, increased cyclic AMP production should have been observed after the treatment with oestradiol.Isoprenaline mimicked the stimulatory action of oestradiol on uterine ornithine decarboxylase. However, this action of isoprenaline was abolished by propranolol, whereas that of oestradiol was only slightly, though significantly, inhibited.The present findings do not support the view that the action of oestradiol on the uterus is mediated by cyclic AMP, and also suggest that \g=b\-adrenergic receptors and PGE2 can have only a minor role, if any, in the mechanism of action of this hormone. * In partial fulfilment of the requirements for the Ph.D. decree of the Graduate School of the Weizmann

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The LOCALIZATION OF [6,7-3h]oestradiol-17β IN RAT UTERUS

Cited by 55 publications

References 10 publications

Antitumor Effects of Droloxifene, a New Antiestrogen Drug, against 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors in Rats

Antitumor Effects of Droloxifene, a New Antiestrogen Drug, against 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors in Rats

The INTRANUCLEAR LOCALIZATION OF [6,7-3h]-Oestradiol-17β IN DIMETHYLBENZANTHRACENE-INDUCED RAT MAMMARY ADENOCARCINOMA AND OTHER TISSUES

MECHANISM OF OESTRADIOL ACTION ON THE RAT UTERUS: INDEPENDENCE OF CYCLIC AMP, PROSTAGLANDIN E2 AND Β-Adrenergic MEDIATION

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