Estrogens/pharmacology* ; Humans ; Smell

Estrogen impacts neural development; meanwhile, it has a protective effect on the brain. Bisphenols, primarily bisphenol A (BPA), can exert estrogen-like or estrogen-interfering effects by binding with estrogen receptors. Extensive studies have suggested that neurobehavioral problems, such as anxiety and depression, can be caused by exposure to BPA during neural development. Increasing attention has been paid to the effects on learning and memory of BPA exposure at different developmental stages and in adulthood. Further research is required to elucidate whether BPA increases the risk of neurodegenerative diseases and the underlying mechanisms, as well as to assess whether BPA analogs, such as bisphenol S and bisphenol F, influence the nervous system.
Receptors, Estrogen/metabolism* ; Estrogens ; Benzhydryl Compounds/pharmacology* ; Nervous System/metabolism*

OBJECTIVETo study 17β-estradiol (E2), ethinylestradiol (EE2), estriol (E3), estrone (E1) on MCF-7 proliferation effects, and compare the effects of independent action (IA) model with concentration addition (CA) model in assessing the combined effects of estrogen.

METHODSThe combinations of E2 + EE2, E2 + E3 and E2 + E1 were chosen and the cellular proliferation effects were examined by MTT assay.

RESULTSThe maximum proliferation effects at dose of 10⁻⁹ mol/L was 325.48% for E2, 330.34% for EE2, 255.22% for E3, and 199.61% for E1. In the E2 + EE2, E2 + E3, E2 + E1 groups, the results of IA model analysis were very close to the experimental results. The IA model tend to overestimated the experimental results, while the CA model often underestimated the experimental results. In the EC (E2, 30) + C (EE2, 70) group, the results exceed the maximum estrogen effects of E2, while in other groups, the results were lower.

CONCLUSIONSThe estrogenic effects of the four tested substances from high to low efficiency were that: EE2 > E2 > E3 > E1. The effect of IA model in predicting the combined effects of binary mixture was better than CA model. A small proportion of binary mixture showed synergy.

Cell Line, Tumor ; Cell Proliferation ; drug effects ; Estradiol ; pharmacology ; Estriol ; pharmacology ; Estrogens ; pharmacology ; Estrone ; pharmacology ; Ethinyl Estradiol ; pharmacology ; Female ; Humans

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

Bone Resorption ; China ; Cytokines ; physiology ; Diphosphonates ; pharmacology ; Estrogens ; pharmacology ; Humans ; Jaw ; drug effects ; metabolism

Estrogen replacement therapy in postmenopausal women may reduce the risk of Alzheimer's disease, possibly by ameliorating neuronal degeneration. In the present study, we examined the neuroprotective spectrum of estrogen against excitotoxicity, oxidative stress, and serum-deprivation-induced apoptosis of neurons in mouse cortical cultures. 17beta-estradiol as well as 17alpha-estradiol and estrone attenuated oxidative neuronal death induced by 24 hr exposure to 100 microM FeCl2, excitotoxic neuronal death induced by 24 hr of exposure to 30 microM N-methyl-D-aspartate (NMDA) and serum-deprivation induced neuronal apoptosis. Furthermore, estradiol attenuated neuronal death induced by Abeta25-35. However, all these neuroprotective effects were mediated by the anti-oxidative action of estrogens. When oxidative stress was blocked by an antioxidant trolox, estrogens did not show any additional protection. Addition of a specific estrogen receptor antagonist ICI182,780 did not reverse the protection offered by estrogens. These findings suggest that high concentrations of estrogen protect against various neuronal injuries mainly by its anti-oxidative effects as previously shown by Behl et al. Our results do not support the view that classical estrogen receptors mediate neuroprotection.
Amyloid beta-Protein/pharmacology ; Animal ; Antioxidants/pharmacology* ; Antioxidants/metabolism ; Apoptosis/drug effects* ; Cells, Cultured ; Chelating Agents/pharmacology ; Chromans/pharmacology ; Estradiol/pharmacology ; Estrogens/pharmacology* ; Estrogens/metabolism ; Estrone/pharmacology ; Ethylenediamines/pharmacology ; Excitatory Amino Acid Agonists/pharmacology ; Ferric Compounds/pharmacology ; Lactate Dehydrogenase/analysis ; Mice ; N-Methylaspartate/pharmacology ; Neurons/metabolism ; Neurons/drug effects* ; Neurons/cytology ; Organ of Corti/cytology ; Peptide Fragments/pharmacology ; Staurosporine/pharmacology

Estrogen replacement therapy in postmenopausal women may reduce the risk of Alzheimer's disease, possibly by ameliorating neuronal degeneration. In the present study, we examined the neuroprotective spectrum of estrogen against excitotoxicity, oxidative stress, and serum-deprivation-induced apoptosis of neurons in mouse cortical cultures. 17beta-estradiol as well as 17alpha-estradiol and estrone attenuated oxidative neuronal death induced by 24 hr exposure to 100 microM FeCl2, excitotoxic neuronal death induced by 24 hr of exposure to 30 microM N-methyl-D-aspartate (NMDA) and serum-deprivation induced neuronal apoptosis. Furthermore, estradiol attenuated neuronal death induced by Abeta25-35. However, all these neuroprotective effects were mediated by the anti-oxidative action of estrogens. When oxidative stress was blocked by an antioxidant trolox, estrogens did not show any additional protection. Addition of a specific estrogen receptor antagonist ICI182,780 did not reverse the protection offered by estrogens. These findings suggest that high concentrations of estrogen protect against various neuronal injuries mainly by its anti-oxidative effects as previously shown by Behl et al. Our results do not support the view that classical estrogen receptors mediate neuroprotection.
Amyloid beta-Protein/pharmacology ; Animal ; Antioxidants/pharmacology* ; Antioxidants/metabolism ; Apoptosis/drug effects* ; Cells, Cultured ; Chelating Agents/pharmacology ; Chromans/pharmacology ; Estradiol/pharmacology ; Estrogens/pharmacology* ; Estrogens/metabolism ; Estrone/pharmacology ; Ethylenediamines/pharmacology ; Excitatory Amino Acid Agonists/pharmacology ; Ferric Compounds/pharmacology ; Lactate Dehydrogenase/analysis ; Mice ; N-Methylaspartate/pharmacology ; Neurons/metabolism ; Neurons/drug effects* ; Neurons/cytology ; Organ of Corti/cytology ; Peptide Fragments/pharmacology ; Staurosporine/pharmacology

To evaluate the estrogenic activities of several chemicals such as 17 beta-estradiol (E2), rho-nonylphenol, bisphenol A, butylparaben, and combinations of these chemicals, we used recombinant yeasts containing the human estrogen receptor [Saccharomyces cerevisiae ER + LYS 8127]. We evaluated E2 was most active in the recombinant yeast assay, followed by rho-nonylphenol, bisphenol A, butylparaben. The combinations of some concentrations of 17-estradiol as a strong estrogen and bisphenol A or butylparaben as a weak estrogen showed additive estrogenic effects. Also, the combinations of some concentrations of nonlyphenol and butylparaben and combination of butylparaben and bisphenol A showed additive effects in the estrogenic activity. Therefore, the estrogenic activities of the combinations of two chemicals were additive, not synergistic.
Cloning, Molecular ; Estradiol/pharmacology ; Estrogens/classification/*pharmacology ; Estrogens, Non-Steroidal/*pharmacology ; Humans ; Kinetics ; Parabens/pharmacology ; Phenols/pharmacology ; Receptors, Estrogen/drug effects/*physiology ; Recombinant Proteins/drug effects/metabolism ; Saccharomyces cerevisiae/genetics

BACKGROUNDThere are definite gender differences in patients with macular holes. Menopausal women over 50 years are most affected. We aimed to observe the effect of estrogen on collagen gel contraction by cultured human retinal glial cells. It is speculated that estrogen could strengthen the tensile stress of the macula by maintaining the correct morphology and contraction.

METHODSEstrogen was used to determine its effects on collagen gel contraction, and its function was measured using morphological changes in cells. Human retinal glial cells were cultured in collagen solution. The cells were then exposed to collagen gels and the degree of contraction of the gel was determined.

RESULTSEstrogen at differing concentrations had no effect on the growth of human retinal glial cells. However, after exposed to collagen gel block, less contraction was noted in the estrogen-treated group than in the control group.

CONCLUSIONSEstrogen can inhibit collagen gel contraction by glial cells. These results suggest a mechanism for macular hole formation, which is observed in menopausal females.

Cells, Cultured ; Collagen ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Estrogens ; pharmacology ; Female ; Humans ; Neuroglia ; drug effects ; metabolism

OBJECTIVETo review the recent developments in the mechanisms of epithelium sodium channels (ENaCs) induced bone formation and regulation.

DATA SOURCESStudies written in English or Chinese were searched using Medline, PubMed and the index of Chinese-language literature with time restriction from 2005 to 2014. Keywords included ENaC, bone, bone formation, osteonecrosis, estrogen, and osteoporosis. Data from published articles about the structure of ENaC, mechanism of ENaC in bone formation in recent domestic and foreign literature were selected.

STUDY SELECTIONAbstract and full text of all studies were required to obtain. Studies those were not accessible and those did not focus on the keywords were excluded.

RESULTSENaCs are tripolymer ion channels which are assembled from homologous α, β, and γ subunits. Crystal structure of ENaCs suggests that ENaC has a central ion-channel located in the central symmetry axis of the three subunits. ENaCs are protease sensitive channels whose iron-channel activity is regulated by the proteolytic reaction. Channel opening probability of ENaCs is regulated by proteinases, mechanical force, and shear stress. Several molecules are involved in regulation of ENaCs in bone formation, including nitride oxide synthases, voltage-sensitive calcium channels, and cyclooxygenase-2.

CONCLUSIONThe pathway of ENaC involved in shear stress has an effect on stimulating osteoblasts even bone formation by estrogen interference.

Calcium Channels ; physiology ; Epithelial Sodium Channels ; chemistry ; physiology ; Estrogens ; pharmacology ; Humans ; Osteogenesis ; physiology