No Abstract Available.
Estrogens*

No abstract available.
Estrogens*

No abstract available.
Estrogens*

It is known that inflammatory processes result from intraocular surgery or ocular trauma mediated by prostaglandin, which cause the protein amounts to increase in anterior chmaber, congestion of vessels, miosis and intraocular pressure to increase. In order to compare the anti-inflammatory effects of antiprostaglandin agents such as Aspegic(R), Profenal(R) and Ocufen(R) in 40 eyes of 20 rabbits, we measured the pupil diameter and amounts of PG E2 and total protein before and after paracentesis. The inhibitory effects of Aspegiz(R), Profenal(R) and Ocufen(R) to pupillary constnztion were significantly greater (p<0.05) than control. The lowering effect to PG E2 and total protein were greater in Aspegic(R), Profenal(R) and Ocufen(R) than control. Through over experiment we suggested that the topical non-steroidal anti-inflammatory agents such as Aspegic(R), Profenal(R), and Ocufen(R) can inhibit the PG activator in antivator chamber and interrupt the miosis and rising intraocular pressure during surgery.
Anterior Chamber* ; Anti-Inflammatory Agents, Non-Steroidal* ; Estrogens, Conjugated (USP) ; Intraocular Pressure ; Miosis ; Paracentesis* ; Pupil ; Rabbits*

OBJECTIVETo explore the effects of environmental estrogens (n-4-noniphenol, NP; bisphenol, BisA; and dibutylphthalate, DBP) on apoptosis induced by estrogen depletion in breast cancer T47D cells.

METHODSHuman T47D breast cancer cells were grown in DMEM medium containing 10% bovine serum. Four days before adding the test compounds, the cells were washed in phosphate-buffered saline, and the medium was substituted with a phenol red-free DMEM medium containing 5% dextral charcoal-stripped FBS. Respective test compound was added in fresh medium and the control cell received only the vehicle (ethanol). Apoptotic features in T47D cell were analyzed by light microscope that was commonly used to define apoptosis. DNA integrity of T47D cells was examined by agarose gel electrophoresis. Hypodiploid population was detected by flow cytometry.

RESULTSThe typical characters of apoptosis in T47D cells were observed after estrogen deletion and then disappeared following exposure to T47D cells at 32 x 10(-7) mol/L Np and 32 x 10(-7) mol/L BisA respectively. Inhibition of apoptosis at 32 x 10(-6) mol/L DBP was not shown in our study.

CONCLUSIONN-4-noniphenol and Bisphenol A could inhibit apoptosis induced by estrogen deletion in breast cancer T47D cells. This result suggests that these environmental estrogens might involve in signal transduction connected with apoptosis.

Apoptosis ; drug effects ; Benzhydryl Compounds ; Cell Line, Tumor ; drug effects ; metabolism ; Dibutyl Phthalate ; pharmacology ; Estrogens ; deficiency ; Estrogens, Non-Steroidal ; pharmacology ; Female ; Flow Cytometry ; Humans ; Phenols ; pharmacology

OBJECTIVETo study the effects of phytoestrogen alpha-zearalanol (alpha-ZAL) on normal human breast.

METHODSTen specimens of normal human breast tissues were subcutaneously implanted into 30 athymic nude mice aged 9-10 weeks, one for 3 mice. These mice were then randomly divided into three groups: control group (without hormone treatment, n = 10), 1 mg/kg alpha-ZAL group (n = 10), and 5 mg/kg alpha-ZAL group (n = 10). All breast tissues were taken out 6 weeks later. Immunohistochemistry was used to determine the protein expressions of proliferating cell nuclear antigen (PCNA), inhibiting apoptosis gene Bcl-2, estrogen receptor (ER), and progesterone receptor (PR). Reverse transcription polymerase chain reaction (RT-PCR) was used to measure the expression levels of estrogen sulfotransferase (EST) mRNA and bridging integrator protein-1 (BIN1) mRNA. Morphological features of grafts before and after treatment were also observed.

RESULTSAlpha-ZAL had no significant effects on Bcl-2, PCNA, ER, and PR expression of mammary epithelial cells in graft specimens. Alpha-ZAL upregulated BIN1 mRNA expression in grafts, but had no significant effect on ESTmRNA expression.

CONCLUSIONSAlpha-ZAL does not affect the morphology, proliferating, and apoptosis of epithelial cells in normal human breast tissues implanted into nude mice, but it may increase the gene expression of tumor-inhibiting BIN1, suggesting that alpha-ZAL may have potential proteotive effect on normal human breast.

Adult ; Animals ; Breast ; chemistry ; drug effects ; Estrogens, Non-Steroidal ; pharmacology ; Female ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Phytoestrogens ; pharmacology ; Proliferating Cell Nuclear Antigen ; analysis ; Random Allocation ; Receptors, Estrogen ; analysis ; Receptors, Progesterone ; analysis ; Zeranol ; pharmacology

The cardiac electrophysiological effects of genistein (GST) were examined in guinea pig papillary muscle using intracellular microelectrode technique. The results obtained are as follows. (1) Duration of action potential (APD) in normal papillary muscles was decreased by GST (10 100 micromol/L) in a concentration-dependent manner. (2) In partially depolarized papillary muscles, 50 micromol/L GST not only reduced APD, but also decreased the amplitude of action potential, overshoot and maximal velocity of phase 0 depolarization. (3) Pretreatment with N( )-nitro-L-arginine (L-NNA, 5 mmol/L) failed to affect the above effects of GST (50 micromol/L)on papillary muscles. (4) 17beta-estradiol (E(2), 5 micromol/L) or GST (10 micromol/L) alone did not affect action potential, while GST combined with E(2) at the same doses shortened APD significantly. All these results indicate that the effects of GST on papillary muscles are likely due to a decrease of calcium inflow which is not mediated by NO and that GST has a facilitative or synergetic action with E(2).
Action Potentials ; drug effects ; Agmatine ; pharmacology ; Animals ; Dose-Response Relationship, Drug ; Drug Synergism ; Electrophysiology ; Estradiol ; pharmacology ; Estrogens, Non-Steroidal ; pharmacology ; Female ; Genistein ; pharmacology ; Guinea Pigs ; Isoflavones ; Male ; Papillary Muscles ; drug effects ; physiology ; Phytoestrogens ; Plant Preparations

Animals ; Coronary Disease ; prevention & control ; Dibutyl Phthalate ; adverse effects ; Dioxins ; adverse effects ; Environmental Pollutants ; adverse effects ; Estrogens, Non-Steroidal ; pharmacology ; Humans ; Isoflavones ; pharmacology ; Phytoestrogens ; Plant Preparations ; pharmacology ; Zearalenone ; adverse effects

No abstract available.
Breast* ; Estrogens*

No abstract available.
Adenocarcinoma* ; Estrogens*