Estrogen–androgeri interaction: selective inhibition of estrogen-induced uterine peroxidase by testosterone and 5α-dihydrotestosterone

1983 ◽  
Vol 61 (7) ◽  
pp. 779-783 ◽  
Author(s):  
Peter H. Jellinck ◽  
Andrew Affleck ◽  
Anne-Marie Newcombe
Keyword(s):  
Estrogen Receptor ◽  
Low Dose ◽  
Combined Treatment ◽  
Selective Inhibition ◽  
Time Intervals ◽  
Rat Uterus ◽  
Immature Rat ◽  
Uterine Growth ◽  
Nuclear Estrogen Receptor ◽  
Glucose 6 Phosphate Dehydrogenase

The effect of testosterone (T) and dihydrotestosterone (DHT) on the induction of peroxidase and glucose-6-phosphate dehydrogenase (G6PDH) in the immature rat uterus by estradiol (E2) was investigated. T (0.5–12.5 mg/rat) given on 3 successive days produced a large increase in uterine weight but, in contrast to E2, did not induce peroxidase or significantly augment uterine G6PDH. However, this androgen, even at a very low dose (50 μg/rat three times), inhibited the induction of peroxidase without a corresponding effect on G6PDH when given concurrently with E2 and was more effective than DHT. Inhibition by androgen was also observed when diethylstilbestrol was used to stimulate uterine growth. Combined treatment with E2 (3 μg/rat) and T (3 mg/rat) produced a cytosolic and nuclear estrogen receptor pattern in the uterus similar to that observed with E2 alone after various time intervals. The results speak against a direct inhibitory action or T on E2-induced uterine peroxidase via the estrogen receptor and confirm the lack of aromatization of T to E2 in the immature rat. Possible mechanisms for modifying the action of estrogens by androgens are discussed, particularly in the light of E2-induced eosinophilia. It is proposed that steroid hormones can interact in several ways and that uterine peroxidase provides a useful indicator to study steroid hormone action.

Binding characteristics of 5-androstene-3β, 17β-diol and estradiol-17β to the cytoplasmic estrogen receptor of the immature rat uterus

1982 ◽  
Vol 16 (5) ◽  
pp. 661-671 ◽  
Author(s):  
L.G. Van Doorn ◽  
J. Berenschot-Roozendaal ◽  
J. Poortman ◽  
J.H.H. Thussen ◽  
F. Schwarz
Keyword(s):  
Estrogen Receptor ◽  
Rat Uterus ◽  
Immature Rat ◽  
Binding Characteristics ◽  
Estradiol 17Β

Comparison of the biological effects of tamoxifen and a new antioestrogen (LY 117018) on the immature rat uterus

1983 ◽  
Vol 99 (3) ◽  
pp. 447-453 ◽  
Author(s):  
A. E. Wakeling ◽  
K. M. O'Connor ◽  
E. Newboult
Keyword(s):  
Biological Effects ◽  
Prior Treatment ◽  
Uterine Weight ◽  
Rat Uterus ◽  
Immature Rat ◽  
Uterine Growth ◽  
High Doses

The uterotrophic and antiuterotrophic activities of tamoxifen and 6-hydroxy-2-(p-hydroxyphenyl)-benzo(b)thien-3-yl p- <2-(1-pyrrolidinyl) ethoxyphenyl ketone (LY 117018) in the immature rat uterus have been evaluated. The antioestrogens were administered alone, concurrently or sequentially with or without oestradiol. LY 117018 administered alone was less uterotrophic (oestrogenic) than tamoxifen. At high doses, when administered concurrently with oestradiol, LY 117018 was more antiuterotrophic (antioestrogenic) than tamoxifen. When uterine growth was maximally stimulated by prior treatment with oestradiol, tamoxifen and LY 117018 were equally effective in reducing uterine weight. However, when uterine growth was induced with a dose of oestradiol producing an oestrogenic effect equivalent to that of tamoxifen (but less than that produced by LY 117018) LY 117018 was more effective than tamoxifen in reversing the uterotrophic effect of oestradiol. In animals pretreated with LY 117018 a further increase in uterine weight occurred on treatment with tamoxifen. The increase in uterine weight after tamoxifen was progressively reversed by increasing doses of LY 117018. The hypothesis that tamoxifen and LY 117018 may act by different mechanisms, based on the apparent failure of LY 117018 to antagonize the uterotrophic action of tamoxifen, is not supported by these studies.

scholarly journals The estrogen receptor α Σ3 mRNA splicing variant is differentially regulated by estrogen and progesterone in the rat uterus

2005 ◽  
Vol 186 (1) ◽  
pp. 51-60 ◽  
Author(s):  
J Varayoud ◽  
J G Ramos ◽  
L Monje ◽  
V Bosquiazzo ◽  
M Muñoz-de-Toro ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Alternative Splicing ◽  
Estrous Cycle ◽  
Low Dose ◽  
Estrogen Receptor Α ◽  
Mrna Splicing ◽  
Female Rats ◽  
Rt Pcr ◽  
Mrna Isoforms ◽  
Rat Uterus

The gene for estrogen receptor α (ERα) has been shown to be under complex hormonal control and its activity can be regulated by mRNA alternative splicing. Here we examined the regulation of ERα transcription and translation in the rat uterus by ovarian steroid hormones. We examined whether expression of ERα mRNA splice isoforms is hormonally regulated in ovariectomized (OVX) and cycling rats. Adult OVX female rats were treated daily with 17-β estradiol (E2) (0.05 μg/rat or 5 μg/rat), progesterone (P4) (1 mg/rat) or a combination of both hormones for 4 days. Animals were killed 24 h after the last injection and uterine horns were removed. In order to determine whether ERα mRNA isoforms are differentially expressed under various physiological conditions, animals were evaluated at proestrus, estrus and diestrus. The ERα protein and mRNA were detected by immunohistochemistry and comparative RT-PCR analysis respectively. The presence of ERα mRNA isoforms was evaluated using a nested RT-PCR assay. In OVX control rats, ERα mRNA and protein levels were high, demonstrating a constitutive expression of the ERα gene in the uterus. When animals received P4 or the high dose of E2, a significant decrease in both ERα mRNA and protein was observed in the uterus. However, when rats were protein was treated with the low dose of E2, only the ERα down-regulated; no changes were observed in ERα mRNA expression. In addition to the full-length ERα mRNA, OVX control rat uteri expressed three shorter transcripts: Σ3, Σ4 and Σ3,4 (lacking exon 3, exon 4, or both 3 and 4 respectively). Surprisingly, when OVX animals were treated with P4, the low dose of E2 or a combination of both steroids, expression of the Σ3 isoform was completely abolished. During the estrous cycle, all ERα mRNA splicing variants were detected at proestrus and estrus. However, in diestrus, significant low levels of the Σ3 isoform were observed. In summary, our results suggest a dose-dependent relationship between E2 concentrations and the level of control in the ERα transcription–translation cascade. Moreover, the alternative splicing of the ERα primary transcript is influenced by the hormonal milieu, suggesting that these events could affect the estrogen responsiveness of the rat uterus during the estrous cycle.

scholarly journals Changes in the patterns of synthesis of ribonucleic acid species in immature rat uterus in response to oestradiol-17β

1969 ◽  
Vol 112 (5) ◽  
pp. 563-569 ◽  
Author(s):  
R J Billing ◽  
B Barbiroli ◽  
R. M. S. Smellie
Keyword(s):  
Ribosomal Rna ◽  
Hormone Treatment ◽  
Transfer Rna ◽  
Time Intervals ◽  
Rat Uterus ◽  
Immature Rat ◽  
Oestradiol Treatment ◽  
Wet Weight ◽  
Major Increase ◽  
Rna And Dna

1. After treatment of immature rats with diethylstilboestrol, the wet weight and RNA content of uterine tissue increased rapidly, reaching a peak at 40hr. After an initial lag of a few hours, the acid-soluble ribose and protein contents also rose to maxima at 40hr. No increase in DNA content occurred until at least 24hr. after treatment. 2. The RNA from immature rat uterus isolated at various times up to 6hr. after administration of oestradiol-17β was labelled by injecting [3H]uridine and [3H]guanosine intraperitoneally 30min. before the animals were killed. It was fractionated on columns of kieselguhr coated with methylated serum albumin and the radioactivity in fractions corresponding to transfer RNA, 7s RNA, ribosomal RNA, Q1-RNA, Q2-RNA and DNA-like RNA was determined. 3. The radioactivity of the whole RNA increased steadily for 6hr. after hormone treatment. The earliest changes occurred in the Q1-RNA (ribosomal RNA precursor), whereas at longer time-intervals the radioactivity of the ribosomal RNA, 7s RNA and transfer RNA increased by four- to five-fold. The radioactivity of the DNA-like RNA increased by about 50%, but only at the longer time-intervals. 4. It is concluded that one of the earliest changes in response to oestradiol treatment is a major increase in synthesis of ribosomal RNA followed later by a similar increase in synthesis of transfer RNA and by a much smaller increase in synthesis of DNA-like RNA. The change in synthesis of ribosomal RNA in immature rat uterus may represent one of the most important responses to oestradiol treatment.

scholarly journals Selective Estrogen Receptor Modulation by Larrea nitida on MCF-7 Cell Proliferation and Immature Rat Uterus

2014 ◽  
Vol 22 (4) ◽  
pp. 347-354 ◽  
Author(s):  
Hye-Na Ahn ◽  
Si-Yeon Jeong ◽  
Gyu-Un Bae ◽  
Minsun Chang ◽  
Dongwei Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Rat Uterus ◽  
Immature Rat ◽  
Receptor Modulation ◽  
Mcf 7

EFFECT OF EQUOL ON OESTROGEN RECEPTORS AND ON SYNTHESIS OF DNA AND PROTEIN IN THE IMMATURE RAT UTERUS

1980 ◽  
Vol 85 (2) ◽  
pp. 291-297 ◽  
Author(s):  
B. Y. TANG ◽  
N. R. ADAMS
Keyword(s):  
Subcutaneous Injection ◽  
Female Rats ◽  
Receptor Complex ◽  
Oestrogen Receptors ◽  
Rat Uterus ◽  
Immature Rat ◽  
Nuclear Binding ◽  
Uterine Growth ◽  
Wet Weight

In immature, 3-week-old female rats, 5 mg equol given by subcutaneous injection increased uterine wet weight 24 h later to the same degree as did 5 μg oestradiol-17β. At this dose there was more receptor complex binding to the nucleus in the equol-injected rats than in the rats injected with oestradiol-17β even after 6 h. However, the equol–receptor complex that bound to the nucleus was more extractable with 0·3 m-KC1. In the equol-injected rats the duration of uterine growth was shorter and there was less receptor replenishment and synthesis of protein and DNA than in the rats injected with oestradiol-17β 30 h after either injection. It was concluded that equol is a weakly oestrogenic compound which is antagonistic to oestradiol-17β by competing with oestradiol–receptor complex for nuclear binding and yet fails to initiate the replenishment of oestrogen receptors effectively in the cytoplasm.

scholarly journals Changes in uterine ornithine decarboxylase activity and steroid receptor levels during decidualization in the rat induced by CDRI-85/287

1999 ◽  
pp. 426-430 ◽  
Author(s):  
A Dwivedi ◽  
G Gupta ◽  
G Keshri ◽  
JD Dhar
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptor ◽  
Rat Model ◽  
Treated Group ◽  
Ovariectomized Rats ◽  
Decarboxylase Activity ◽  
Marker Enzyme ◽  
Rat Uterus ◽  
Immature Rat ◽  
Group A

CDRI-85/287 is an anti-estrogen and interferes with decidualization in the rat uterus. In this study, uterine estrogen receptor (ER) and progesterone receptor (PR) levels were determined during the inhibition of decidualization. The effect of 85/287 on uterine ornithine decarboxylate (ODC) activity (a marker enzyme for decidualization) was also studied, using immature ovariectomized rats divided into four different groups: control, 2.5mg/kg 85/287 only; 1 microg estradiol only; and 85/287 + estradiol. Pseudopregnant rats were administered 85/287 (2.5mg/kg p.o.) on day 3 post-coitum. Deciduoma was induced in one of the uterine horns on day 4 and animals were autopsied 18h post-traumatization. Both ERs and PRs showed an increase in traumatized horns compared with non-traumatized. In the 85/287-treated uterus, there was a reduction in cytosolic ERs in both traumatized horns. However, nuclear ER and PR levels increased in both horns under the influence of 85/287. Similarly, in a tamoxifen (0.03mg/kg)-treated group a decline was noticed in cytosolic ER with a mild increase in nuclear PR. Total ER content, expressed per 100 microg DNA, showed a decline in 85/287- or tamoxifen-treated rats. However, no significant alterations were observed in total PR levels in non-traumatized horns. In an immature rat model, 85/287 caused a significant (>50%) reduction in estradiol-induced ODC activity. These findings suggest that the decidualization inhibitory activity of 85/287 may be attributed to inhibition of certain timed biochemical events and genomic/non-genomic actions of estrogens in the rat uterus.

Sign in / Sign up

Export Citation Format

Share Document