• Korean Journal of Veterinary Research
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• v.27 no.1
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• pp.9-17
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• 1987

The present study has been carried out to elucidate the antiestrogenic effects of tamoxifen in immature rat uterus. The content of DNA and protein and uterine wet weight were measured after the injections of $5{\mu}g$ of estradiol-$17{\beta}$, $50{\mu}g$ of tamoxifen, a combination of both, or vehicle only subcutaneously. The results obtained were summarized as follows: 1. DNA content in uterus was increased at 48 hours after estradiol-$17{\beta}$ or tamoxifen injection (p<0.01). 2. The increament rate of uterine DNA content was significantly (p<0.01) lower in tamoxifen treated group than that in estradiol-$17{\beta}$ treated group. 3. Antiestrogenic effect of tamoxifen on protein content in uterus was apparent at 72 hours after simultaneous administration of both drugs. 4. The uterine wet weight was started to increase at three hours after the injection of estradiol-$17{\beta}$ or tamoxifen. 5. While estradiol-$17{\beta}$ increased steadily uterine wet weight up to 138.5mg at 72 hours after the injection, but tamoxifen failed to increase it after 48 hours. Tamoxifen inhibited significantly (p<0.01) the effect of estradiol-$17{\beta}$ on it thereafter.

• Advances in Traditional Medicine
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• v.7 no.2
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• pp.114-120
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• 2007

In the present study, the hydro alcoholic extract of Moringa concanensis and their different fractions were evaluated for it's anti implantation, abortifacient, estrogenic and antiestrogenic activity. Hydro alcoholic extract of Moringa concanensis has showed potent antiimplantation and abortifacient activity at 200 mg/kg and 400 mg/kg respectively and marked estrogenic activity when administered individually and anti estrogenic activity was observed when administered along with ethinyl estradiol (1 ${\mu}g/rat/day$) as well as their different fractions of Moringa concanensis showed significant antiimplantation and abortifacient activity at 100 mg/kg. Moreover, all tested fractions showed significant anti estrogenic activity when administered simultaneously with ethinyl estradiol.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.166-166
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• 2002

In the present study, estrogenic or antiestrogenic activity of cypermethrin, a pyrethroid insecticide was investigated. We used immature rat uterotrophic assay, estrogen-responsive calbindin-D9k (CaBP-9k) gene expression assay and luciferase reporter gene assay for measure of estrogenic potential of cypermethrin.(omitted)

• Korean Journal of Veterinary Research
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• v.25 no.2
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• pp.187-195
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• 1985

The Present study has been carried out to elucidate the antiestrogenic effects of tamoxifen in uteri of immature rats. Immature female Sprague-Dawley rats were allocated into 4, groups and injected with $5{\mu}g$ of estradiol-$17{\beta}$, $50{\mu}g$ of tamoxifen, a combination of both or vehicle only subcutaneously three times after an interval of 24 hours respectively. The concentrations, of cytosol estradiol receptor in uterus were measured by DCC method before and 1, 3, 6, 12, 24, 48 and 72 hours after the above treatments and those of nuclear estradiol were measured by protamine exchange method 72 hours and those of nuclear estradiol were measured by protamine exchange method 72 hours after the above treatments. The results obtained were summarized as follows: 1. The binding affinity of tamoxifen to estradiol receptor in uterine cytosol was lower than that of estradiol-$17{\beta}$, accordingly the translocation of estradiol receptor into the nucleus was found to be delayed. 2. Tamoxifen caused the retention of estradiol receptor in nucleus over 24 hours and inhibited the replenishment of the receptor from nucleus to cytosol in uterus.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.296.2-296.2
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• 2002

Our previous study demonstrated that 2.3', 4.4'. 5- Pentachlorobiphenyl (PCB 118) showed an antiestrogenic activity in vitro and in vivo. In the present study. we examined the effect of PCB 118 on postnatal reproductive development in female rats. PCB 118 (0.001. 0.01 or 0.1 mg/kg/day) was administered to pregnant female SD rats from gestation day (GO) 6 to 18 via subcutaneous injection. and developmental parameters such as vaginal opening were determined. PCB 118 significantly delayed vaginal opening of female offsprings at dose of 0.1 ${\mu}g$/kg/day. whereas had no effects on body weights. In addition. in utero treatment of PCB 118 caused significant decreases in serum levels of E2, T3 and T4 in female oftsprings at certain doses on postnatal day (PND) 22. Our data of results indicate that in utero exposure to PCB 118 may postnatal reproductive development in female rat through its antiestrogenic activity.

• Korean Journal of Veterinary Research
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• v.26 no.1
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• pp.31-37
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• 1986

The present study has been carried out to elucidate the antiestrogenic effects of tamoxifen on RNA and protein synthesis in uteri of immature rats. Immature female Sprague-Dawley rats were allocated into 4 groups and injected with $5{\mu}g$ of estradiol-$17{\beta}$, $50{\mu}g$ of tamoxifen, a combination of both, or vehicle only subcutaneously three times with an interval of 24 hours respectively. The specific activities of $^3H$-uridine incorporation into uterine RNA and those of $^3H$-leucine incorporation into uterine protein were measured before and 1, 3, 6, 12, 24, 48 and 72 hours after the above treatments. The results obtained were summarized as follows; 1. Tamoxifen itself increased RNA synthesis an hour after treatment(169.18% of control), but it's specific activity was reduced to control level after 3 hours. Tamoxifen inhibited significantly (p<0.01) the activity of RNA synthesis of estradiol-$17{\beta}$. 2. The increasing rate of protein synthesis was lower in tamoxifen treated group than that in estradiol-$17{\beta}$ treated group. While the rate was steadily increased up to 357.4% of control by estradiol-$17{\beta}$ in 72 hours, tamoxifen itself failed to increase the rate after 24 hours and significantly (p<0.01) inhibited the activity of estradiol-$17{\beta}$(-167.4%).

• Archives of Pharmacal Research
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• v.29 no.5
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• pp.354-362
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• 2006

Dietary flavonoids have attracted a great deal of attention as agents for preventing estrogen-related diseases, such as postmenopausal symptoms, and for reducing the risk of estrogen-dependent cancer. Kaempferol is one of the most commonly found dietary phytoestrogen. The aim of this study was to investigate the estrogenic and/or antiestrogenic effect of kaempferol, which can confirm its potency as a preventive agent against estrogen-related diseases. Kaempferol has both estrogenic and antiestrogenic activity, which are biphasic response on estrogen receptor. The estrogenic activity of kaempferol induced via ER-mediated pathway depending on $E_2$ concentration $(\leq\;10^{-12}M)$. Kaempferol $(10^{-5}\;M)$ also caused antiproliferative effect on MCF-7 cell in the presence of $E_2\;(10^{-11}\;M)$ and restored to the addition of excess $E_2\;(10^{-7}\;M)$, which confirms that antiproliferation of kaempferol was induced via ER-dependent pathway. However, at $10^{-4}\;M$, concentration higher than the concentrations at which the estrogenic effects of kaempferol are detected $(10^{-5}\;M)$, kaempferol induced strong antiproliferative effect, but were unaffected by the addition of excess $E_2\;(10^{-7}\;M)$ indicating that kaempferol exerts antiproliferation via ER-independent pathway. In particular, kaempferol blocked the focus formation induced by $E_2$, which confirms that kaempferol might inhibit the malignant transformation caused by estrogens. Therefore, we suggested that kaempferol might regulate a suitable level of estrogenic activity in the body and is expected to have potential beneficial effects in preventing estrogen imbalance diseases (breast cancer, osteoporosis, cardiovascular disease and etc.).

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.3
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• pp.521-526
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• 2002

A number of experimental and epidemiological studies have implicated that antiestrogenic effects of estrogen-like compounds in legumes and plant seeds are responsible for lowering breast cancer risk in human. However, few studies have been conducted to illustrate the possible chemopreventive effects of Korean traditional food materials. This study was performed to determine the cytotoxic and apoptotic effects of yellow soybeans, black soybeans and brown rice extracts on hormone-dependent and hormone-independent human breast cancer cells. Methanol-or acetone-soluble fractions of soybeans or brown rice were incubated with hormone-dependent cells (MCF-7) or hormone-independent cells (MDA-MB-231). Cell cytotoxicity was measured by MTT assay at 24, 48 and 72 hrs of incubation. Apoptotic effects of these extracts toward breast cancer cells were also determined at 48 hrs of incubation by measuring DNA fragmentation. Results indicated that the acetone-soluble fraction of brown rice exerted strongest cytotoxic effect on MCF-7 ceIls, although other fractions also reduced the number of viable MCF-7 cells after 48 hrs of incubation. Both acetone and methanol soluble fractions of all samples exerted a significant cytotoxicity towards MDA-MB-231 cells after 24 hrs of incubation, and acetone and methanol soluble fractions of brown rice were especially effective in these cells. At 48 hrs of incubation, methanol fractions of all three samples induced apopotosis of MDA-MB-231 cells. These results indicate methaol or acetone soluble fractions of yellow soybeans, black soybeans and brown rice induce cytotoxicity in both hormone-dependent and hormone-independent breast cancer cells. Therefore, possible mechanisms of cell cytotoxicity do not necessarily include antiestrogenic effects of soybean or brown rice extract. A possible anticarcinogenic effect of brown rice methanol-soluble fraction may mediated through their apoptotic effect. Further studies are requried to elucidate responsible compounds and mechanisms involved in observed anticarcinogenesis.

• Molecular & Cellular Toxicology
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• v.2 no.1
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• pp.15-20
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• 2006

Genistein is a potent, plant-derived isoflavone that displays estrogenic activity at low concentrations but inhibits proliferation at high amounts. However, the molecular mechanism of genistein is not completely understood. In the present study, the biphasic effects (estrogenic and antiestrogenic activity) of genistein on the growth of MCF-7 cells were identified. Genistein within a low range of concentration, $1-10\;{\mu}M$, stimulated proliferation, while $50-100\;{\mu}M$ caused apoptotic cell death. Additionally, genistein at a low concentration induced estrogen receptor (ER)-mediated gene expression and ER phosphorylation. When pre-treated with PD98059, an MEK inhibitor, ER-mediated gene expression and ER phosphorylation by genistein were noticeably increased. However, the increased gene expression and phosphorylation did not enhance cell proliferation. Moreover, it was observed that ER-mediated signaling performs an important role in the MAPK pathway. The proliferation and apoptosis in genistein-treated MCF-7 cells were partially dependent on the Bcl-2 level. The addition of IC1 182, 780, an estrogen receptor antagonist, inhibited Bcl-2 expression induced by genistein. This study suggests that there is a close relationship between Bcl-2 and the ER signaling pathways in MCF-7 cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.23
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• pp.10067-10070
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• 2015

Background: Unopposed estrogen has a central role in development of endometrial benign, premalignant and malignant lesions. The aim of this study was to evaluate the anti-estrogenic effect of metformin on endometrial histology in comparison with progesterone. Materials and Methods: A total of 43 patients who were referred to our center for abnormal uterine bleeding and had a histologic diagnosis were disordered proliferative endometrium or simple endometrial hyperplasia were included and randomly distributed in two groups treated with metformin (500mg Bid) or megestrol (40mg daily), respectively, for three months. After this period the patients were evaluated by another endometrial biopsy to assess the impact of the two drugs in restoring normal endometrial histology. Results: Our findings revealed that metformin could induce endometrial atrophy in 21 out of 22 patients (95.5%) while this positive response was achieved in only 13 out of 21 patients (61.9%) in the megstrol group. In addition two low grade endometrial carcinomas in the metformin group responded very well. Conclusions: We conclude that metformin could be used as an effective antiestrogenic agent in control of abnormal endometrial proliferative disorders.