• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.191-196
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• 1991

The present study was performed to determine whether estradiol, via cAMP mediation, induces prostaglandin synthesis by modulating phospholipase $A_2$ activity which hydrolyzes phospholipids into arachidonic acids, a precursor for prostaglandin synthesis, during the implantation process in rats. Uterine phospholipase $A_2$ activity was elevated on day 5 of pregnancy when implantation normally occurs in rats. Moreover, phospholipase $A_2$ activity was higher in the implant sites than in the non-implant sites of uterus on day 6. In delayed implantation model, phospholipase $A_2$ activity was increased at 12 hrs after estradiol administration and at 8 hrs after dbcAMP administration. In addition, higher activity of phospholipase $A_2$ was induced by the treatment of estradiol plus theophylline, compared with estradiol-only treated group. The simultaneous treatment of indomethacin with estradiol or dbcAMP did not alter phospholipase $A_2$ activity compared with estradiol or dbcAMP-only treated group although significant suppression was observed in uterine PGE and $PGF_{2{\alpha}}$ concentrations. These results suggest that estradiol or cAMP stimulates uterine phospholipase $A_2$ activity, thereby increasing prostaglandin synthesis during the implantation process in rats.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.27-32
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• 1982

To investigate the relationship between platelet monoamine oxidase activity and serum levels of testosterone and estradiol in schizophrenic patient, 78 chronic patients were compared with 135 normal controls. 1) The monoamine oxidase activity of chronic schizophrenic group was lower than normal group. 2) In normal group, there was no sex difference in monoamine oxidase activity. But in chronic schizophrenic group, the monoamine oxidase activity in male was lower than female. 3) In male schizophrenic group, the serum estradiol level was lower than normal group. 4) In female schizophrenic group, the serum testosterone level was lower than normal group. The significances of relationship between platelet monoamine oxidase activity and sex hormones are discussed.

• Clinical and Experimental Reproductive Medicine
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• v.18 no.1
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• pp.41-48
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• 1991

The present investigation has been undertaken to elucidate the functional role of ovarian steroids on the mechanism of oviduct differentiation during early embryonic development in rat. The activity of alkaline phosphatase (ALPase) was measured in the oviduct tissue under different steroids treatment regime on day 9 pregnancy. The ALPase activity of the oviduct of pseudopregnant rat was compared with that of normal pregnant rat. The results of day 9 pregnancy rat oviduct clearly demonstrated that $17{\beta}-estradiol$ and progesterone were effective in pseudopregnant rat oviduct. In the ovary intact group the ALPase activity was similar in both of normal and pseudopregnant oviduct, but in the $17{\beta}-estradiol$ treated group the ALPase activity in normal pregnancy was significantly higher than that in pseudopregnancy. The effect of estradiol on the normal pregnant rat oviduct was apparently found on day 3 and day 9 pregnancy. This study, therefore, clearly demonstrates that $17{\beta}-estradiol$ is much potent in oviduct tissue differentiation. It is suggested that absence of $17{\beta}-estradiol$ effect on pseudopregnant rat oviduct is due to there is no embryo passing througth the oviduct.

• Asian-Australasian Journal of Animal Sciences
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• v.18 no.11
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• pp.1589-1593
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• 2005

The aim of this study was to investigate the effects of testosterone, 17$\beta$-estradiol, and progesterone on the differentiation of bovine intramuscular adipocytes (BIA). Stromal-vascular (SV) cells were obtained from M. longissimus dorsi of 20 months old Korean (Hanwoo) steers, and were cultured in DMEM containing 5% FBS. The proliferated BIA were induced to differentiate with 0.25 $\mu$M dexamethasone, 0.5 mM 1-methyl-3-isobutyl-xanthine and 10 $\mu$g/ml insulin. During differentiation, the cells were treated with testosterone, 17$\beta$-estradiol, and progesterone at concentrations of $10^{-10}$, $10^{-9}$, and $10^{-8}$ M, respectively, for 12 days. Regardless of its concentration, testosterone remarkably reduced lipid droplets in the cytosol of BIA. On the other hand, 17$\beta$-estradiol and progesterone increased the accumulation of lipid droplets in BIA. Testosterone significantly (p<0.05) decreased GPDH activities with a dose-dependent pattern. 17$\beta$-Estradiol treatment onto BIA during differentiation, however, increased GPDH activity showing the highest activity (11.3 nmol/mg protein/min) at $10^{-10}$ M. Treatment of BIA with progesterone also increased (p<0.05) GPDH activity with the highest activity (13.8 nmol/mg protein/min) at $10^{-9}$ M. In conclusion, the results in the current study suggest that testosterone inhibits differentiation of BIA by suppressing GPDH activity while 17$\beta$-estradiol and progesterone have adverse effects.

• Korean Journal of Environmental Agriculture
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• v.27 no.4
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• pp.447-455
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• 2008

Recombinant yeast estrogenicity (YES) assay was used as a bioanalytical tool in order to screen $17{\beta}$-estradiol in the soil samples collected from different sites of South Korea. Solvent extraction and supercritical fluid extraction (SFE) methods were compared for the extraction of the estradiol from the soils. Most high detection of the estradiol based on YES assay was observed in the soils extracted with methanol. Different types of estrogenic hormones including $17{\beta}$-estradiol were suggested to be possibly exiting in the soils, since the methanol extracts of the soils showed an estrogenic activity that was not observed in the hexane extracts of the soil. SFE extracts showed estrogenic activity in some of the samples but methanol extract showed best activity.

• Biomedical Science Letters
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• v.19 no.2
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• pp.147-152
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• 2013

17-${\beta}$-hydroxysteroid dehydrogenase type 1 ($17{\beta}$-HSD type 1) mediates the reaction of $17{\beta}$-estradiol (E2) production from estrone (E1). Inhibitory effects of curcuminoids on $17{\beta}$-HSD type 1 activity were investigated to find a lead compound for treating estrogen-dependent diseases including breast cancer. Among curcuminoids, demethoxycurcumin showed potent inhibitory effect ($IC_{50}=2.7{\mu}M$) on mouse $17{\beta}$-HSD type 1. Curcuminoids also displayed their inhibitory effects on the production of $17{\alpha}$-estradiol which is a carcinogenic metabolite produced by the enzyme. Bisdemethoxycurcumin ($IC_{50}=1.3{\mu}M$) showed potent inhibitory effect on the $17{\alpha}$-estradiol production by chicken $17{\beta}$-HSD type 1. Curcuminoids did not inhibit ERE transcriptional activity with and without E2. Taken together, curcuminoids can be used for treating and preventing E2-dependent diseases via inhibition on $17{\beta}$-HSD type 1 activity.

• Archives of Pharmacal Research
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• v.17 no.2
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• pp.109-114
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• 1994

The role of sex homones in hepatic lipid peroxidation, and in hepatic adehyde odidase and xanthine oxidase activites were investigated using rat liver homogenates. It was observed that male rt had a significantly greater content of malondialdehyde in liver than female. Among the sex hormones tested, estradiol, one of female hormones, markedly inhibited the formation of lipid peroxides in liver tissues in vitro. Especially, the inhibitory effect of estradiol appeared more remarkably in Fe-induced lipid peroxidation. The hepatic xanthine oxidase activity was decreased about 15% by $10\;^6\;M$ estradiol, wherease, the adehyde oxidase activity was almost completely disappeared at the same concentration of estradiol. It implies that sex differences in lipid peroxidation is attributed to the suppression of radical generating system by estradiol.

• Journal of Periodontal and Implant Science
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• v.30 no.2
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• pp.375-390
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• 2000

The purpose of this study is to evaluate the expression ofIGF-I, considered as the mediator of action of estrogen, and IGF-IA and IGF-IB, alternative slicing form of IGF-I, using $17{\beta}-estradiol$ in MC3T3-E1 cells. We observed the effect on type I collagen and osteopontin gene expression and DNA synthetic activity of MC3T3-E1 cells, added by estrogen, IGF-I and combination and the interactionon proliferation and differentiation of MC3T3-E1 cells. The results were as follows :RT-PCR experiment for observing timedependantIGF-I gene expression patternshowed IGF-IA and IB gene expression in both of control and test group. In these IGF-IA gene expression was appeared predominantly. In control, IGF-I geneexpression level was maintained until 24hr and then decreased gradually. In testgroup, IGF-I gene expression level increased as time goes by. Experiment measuring DNA synthetic activity, as it is added by $17{\beta}-estradiol$, IGF-I and combination, showed that first day , there was the tendency of more increase of synthetic activity in all test group than control but no statical significance(P>0.05), and third day, there was more increase of DNA synthetic activity in $17{\beta}-estradiol$ group and combination group and it was statically significant. (P<0.005) Experiment for observing type I collagen gene expression pattern showed more increase of expression in $17{\beta}-estradiol$ group than control and no significant difference in IGF-I group and combination group. Experiment for observing osteopontin gene expression pattern showed no significant difference in control and test group. In conclusion, $17{\beta}-estradiol$ in MC3T3- E1 cells increased IGF-I gene and DNA synthetic activity simultaneously, therefore it appeared that IGF-I is related to the action of estrogen. Combination treatment of IGF-I and $17{\beta}-estradiol$ has effect on cell proliferation but this effect is lower than IGF-I or $17{\beta}-estradiol$ alone. However, combination treatment has not great effect on type I collagen or osteopontin gene expression thus little effect of cell differentiation.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2002.10a
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• pp.170-170
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• 2002

College of Pharmacy, Ewha womans University, Seoul, 120-750, Korea 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most potent halogenated aromatic hydrocarbon congener that induces expression of several genes including CYP1A1. Exposure to TCDD results in many toxic actions such as carcinogenesis, hepatotoxicity, immune suppression, and reproductive and developmental toxicity. Dramatic differences in dioxin toxicity have been observed between the sexes of some animal species, suggesting hormonal modulation of dioxin action. Many studies have been reported and propose several mechanisms of anti-estrogenic effects of TCDD. In contrast, the effect of estrogen on the regulation of CYP1A1 are not clear at present. There are several reports showing conflicting results. It seems that induction/inhibition of CYP1A1 may be dependent on cell-type and concentration. The purpose of this study was to investigate the regulation of TCDD-induced CYP1A1 gene expression by estradiol and its metabolites. We examined whether estradiol and its metabolites altered TCDD-mediated induction of CYP1A1 enzyme activity. 17 ${\beta}$ estradiol and 16 ${\alpha}$ estriol at non cytotoxic concentrations caused a significant concentration dependent decline of TCDD-induced EROD activity To determine whether reduced EROD activity reflected altered CYP1A1 mRNA expression, we measured CYP1A1 mRNA level by RT-PCR. And to examine whether estradiol and its metabolites have effects on TCDD-induced CYP1A1 gene expression at the transcription level, we also peformed transient transfection with an AhR responsive reporter plasmid containing the 5' flanking region of the human CYP1A1 gene to examine whether estradiol and its metabolites have effects on TCDD-induced CYP1A1 gene expression at the transcription level.

• Journal of Embryo Transfer
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• v.3 no.1
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• pp.13-23
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• 1988

These studies were undertaken to examine the interaction of tamoxifen with sex steroid hormones in rat uterine activity. The uterine wet weights of the immature Tat uterus were examined after the administration of estradiol-l7$\beta$(1$\mu$g), tamoxifen(50$\mu$g), progesterone(lmg). The uterotropic activity in immature ovariectomized rats was observed under various treatment conditions following pretreatment with above drugs. The results obtained were as follows:1) Tamoxifen produced significant increase (p <0.01) in uterine wet weight compared with control group, although the increase was not as great as that seen with estradiol-17$\beta$. Administration of estradiol-17$\beta$ together with tamoxifen inhibited significantly the increase of uterine wet weight by estradiol-17$\beta$ (p < 0.01). Coadministration of progresterone with tamoxifen partly blocked the increase of tamoxifen-induced uterine wet weights by progesterone. 2) Estradiol-17$\beta$after the estradiol-17$\beta$ pretreatment discontinued the declining uterine wet weights due to the absence of estrogen support, but uteri continued to increase in weight if daily estradiol-17 $\beta$ was maintained. Administration of tamoxifen on the fourth day of estradiol-17$\beta$ treatment reduced uterine wet weights within 24 hours, and the weights continued to decline with additional tamoxifen. 3) The modest growth of the uterus induced by three daily injections of 5Opg tamoxifen remained stable for five days, with or without additional tamoxifen treatment. Coadministration of tamoxifen with estradiol17$\beta$ increased slightly the increase of uterine wet weight by tamoxifen. Coadministration of tamoxifen with progesterone inhibited the increase of uterine wet weight by tamoxifen. 4) The modest growth of the uterus induced by three daily injections of lmg progesterone reduced uterine wet weight to the control level for five days. Commencement of tamoxifen or estadiol-17 $\beta$ injections on the fourth day of progesterone treatment rapidly elevated uterine wet weight.