Androgen receptor-mediated inhibition of estrogen-induced uterine peroxidase

Jellinck, Peter H.; Newcombe, Anne-Marie

doi:10.1016/0022-4731(83)90348-5

Cited by 12 publications

(5 citation statements)

References 28 publications

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“…The androgen receptor agonist dihydrotestosterone competed ( 3 H)-R 5020 binding with a lower affi nity than did levonorgestrel (IC50 = 2.85 × 10 − 7 M), whereas the antagonist hydroxyfl utamide was a very weak competitor (IC50 = 2.69 × 10 − 5 M, ᭹ ᭤ Fig. 1B ), as already described [17] . Finally, the determination of androgen receptors using ( 3 H)dihydrotestosterone as ligand showed values of 30.4 ± 4.5 fmol / mg prot, which were higher than those we described before using ( 3 H)-testosterone [13] .…”

Section: And Experiments 1: Steroid Receptor Competition Assayssupporting

confidence: 77%

Levonorgestrel Antagonism on Estrogen-induced Pituitary Tumors Is Mediated by Progesterone Receptors

Eb¹,

Grillo²,

Pietranera³

et al. 2008

Horm Metab Res

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Using both IN VITRO and IN VIVO approaches, we studied the antagonism exerted by the synthetic progestin levonorgestrel on estrogen-induced prolactinomas, considering that levonorgestrel shows partial androgenic properties and that androgens inhibit estrogen-induced prolactin synthesis and secretion. In the tumors, binding of estrogens to their receptors was competed neither by progesterone receptor ligands nor by androgen receptor ligands, ruling out direct inhibitory effects of these drugs on tumor development. Progestin binding was competed by the progesterone receptor agonists progesterone and levonorgestrel, by the antagonist mifepristone, and also by the androgen dihydrotestosterone, whereas the androgen receptor antagonist hydroxyflutamide was a weak competitor. In addition, both progesterone receptor and androgen receptor ligands competed for binding to androgen receptors. In primary cultures of pituitary tumors, levonorgestrel decreased prolactin secretion, an effect that was blocked by mifepristone but not by hydroxyflutamide. IN VIVO results indicated that levonorgestrel inhibition of both estrogen-induced pituitary weight increment and hyperprolactinemia was reduced by mifepristone, whereas flutamide was unable to block levonorgestrel effects. Our results suggest that even when an interaction of levonorgestrel with androgen receptors in the tumors is possible, the antagonistic effects of levonorgestrel on tumor development and functionality are mediated by progesterone receptors.

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Section: And Experiments 1: Steroid Receptor Competition Assayssupporting

confidence: 77%

Levonorgestrel Antagonism on Estrogen-induced Pituitary Tumors Is Mediated by Progesterone Receptors

Eb¹,

Grillo²,

Pietranera³

et al. 2008

Horm Metab Res

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“…Whether this effect of androgens on ER can be extended to other cell lines and tissues deserves further study, in light of the fact that androgens specifically antagonize estrogenic action in several systems, in which no mechanism has yet been presented to account for their effect (6,13,46,47,66).…”

Section: Discussionmentioning

confidence: 96%

Down-Regulation of Estrogen Receptors by Androgens in the ZR-75-1 Human Breast Cancer Cell Line*

et al. 1989

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Much clinical evidence indicates that androgens have beneficial effects in the treatment of breast cancer in women. Physiological concentrations of androgens strongly inhibit both basal and estrogen-induced cell proliferation in the human breast cancer cell line ZR-75-1 through their interaction with the androgen receptor. The present study shows that androgens strongly suppress estrogen receptor (ER) and progesterone receptor contents in this model, as measured by radioligand binding and anti-ER monoclonal antibodies. Similar inhibitory effects are observed on the levels of ER messenger RNA (mRNA) measured by ribonuclease protection assay. The androgenic effect is observed at subnanomolar concentrations of the nonaromatizable androgen 5 alpha-dihydrotestosterone, regardless of the presence of estrogens, and is competitively reversed by the antiandrogen hydroxyflutamide. Such data on ER expression provide an explanation for at least part of the antiestrogenic effects of androgens on breast cancer cell growth and moreover suggest that the specific inhibitory effects of androgen therapy could be additive to the standard treatment limited to blockade of estrogens by antiestrogens.

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“…The other, indirect pathway may include the influence of Tarn on different endogenous hormone levels, such as those of gonadotropins and Te (Nagy and Berczi, 1986). Flutomide is a drum that has been shown to exhibit only antiandrogenic activity in humans (Joensuu et ah, 1986;Marugo et ah, 1992) and to exert its action via the androgen receptor (Jellinck and Newcombe, 1983;Keisler et ah, 1991). In our experiments, Flu did not have any effect on the reproductive system in experimental lines, as compared with TP.…”

Section: Discussionmentioning

confidence: 97%

Effects of Gonadal Steroids and Their Antagonists on the Humoral Immune Response of Immune-Selected Broiler Chicks

et al. 1996

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The effects of gonadal hormones, testosterone (Te) and estrogen (E2) as factors in the development of the immune system in two lines, high response (HC) and low response (LC), of broiler chickens divergently selected for early or late immune maturation were studied. For this purpose, plasma Te and E2 levels were tested and correlated with immune response. Also, the effects of exogenous administration of gonadal steroids testosterone propionate (TP), dihydrotestosterone (DHT), and estradiol 3-benzoate (EB), and the nonsteroidal androgen antagonist flutomide (Flu) and anti-estrogen tamoxifen (Tam) on the immune system were studied. Male chicks of the LC line had a higher level of endogenous Te during first 30 d posthatch. The administration of TP or DHT had no noticeable effect on the humoral immune response, whereas DHT suppressed growth of the bursa of Fabricius of both sexes of HC line. No differences in the endogenous E2 level were observed between sexes in either line. Administration of EB inhibited comb and testicle growth and enhanced significantly the humoral immune response to Escherichia coli and sheep erythrocytes (SRBC). The anti-androgen Flu and anti-estrogen Tam strongly inhibited humoral immune response to E. coli and SRBC antigen, whereas no effects on comb and testicle growth were observed. The experimental results suggest that gonadal hormones have similar principal posthatch effects in avian as in mammals; however, the gonadal steroids prehatch effects and the genetic-physiological-environmental effects require further study.

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Androgen receptor-mediated inhibition of estrogen-induced uterine peroxidase

Cited by 12 publications

References 28 publications

Levonorgestrel Antagonism on Estrogen-induced Pituitary Tumors Is Mediated by Progesterone Receptors

Levonorgestrel Antagonism on Estrogen-induced Pituitary Tumors Is Mediated by Progesterone Receptors

Down-Regulation of Estrogen Receptors by Androgens in the ZR-75-1 Human Breast Cancer Cell Line*

Effects of Gonadal Steroids and Their Antagonists on the Humoral Immune Response of Immune-Selected Broiler Chicks

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