piperidines and 2-2-bis(4-hydroxyphenyl)-1-1-1-trichloroethane

piperidines has been researched along with 2-2-bis(4-hydroxyphenyl)-1-1-1-trichloroethane* in 1 studies

Other Studies

1 other study(ies) available for piperidines and 2-2-bis(4-hydroxyphenyl)-1-1-1-trichloroethane

Article	Year
Activation of a uterine insulin-like growth factor I signaling pathway by clinical and environmental estrogens: requirement of estrogen receptor-alpha. Endocrinology, 2000, Volume: 141, Issue:9 Recent data indicate that insulin-like growth factor I (IGF-I) may have a function in mediating the mitogenic effects of 17beta-estradiol (E2) in the uterus and in regulating the growth of uterine neoplasms. This study was designed to determine whether synthetic and plant-derived chemicals that interact with estrogen receptor-alpha (ERalpha) and elicit estrogenic responses also mimic E2 by activating the uterine IGF-I signaling pathway. Ovariectomized adult female mice were treated with both environmental and clinically relevant chemicals previously reported to display estrogenic and/or antiestrogenic properties, and their uteri were evaluated for an activated IGF-I signaling pathway. Diethylstilbestrol, 4-hydroxytamoxifen, the raloxifene analog LY353381, 2,2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane (HPTE), bisphenol A, and genistein were shown to mimic E2 in the uterus by increasing the level of IGF-I messenger RNA, inducing IGF-I receptor (IGF-IR) tyrosine phosphorylation, stimulating the formation of IGF-IR signaling complexes, and increasing both proliferating cell nuclear antigen expression and the number of mitotic cells in the epithelium. The dose of chemical necessary to activate IGF-I signaling varied, with the order of potency: E2 = diethylstilbestrol > LY353381 > 4-hydroxytamoxifen > genistein > HPTE > bisphenol A. Administration of the chemicals to ERalpha knockout mice did not activate IGF-IR, indicating that ERalpha is required for activation of uterine IGF-IR by these diverse chemicals. This study demonstrates that several chemicals shown previously to display estrogenic activities also mimic E2 by activating uterine IGF-I signaling. Topics: Animals; Benzhydryl Compounds; Blotting, Northern; Estradiol Congeners; Estrogen Antagonists; Estrogen Receptor alpha; Estrogens; Estrogens, Non-Steroidal; Female; Insulin-Like Growth Factor I; Mice; Mice, Knockout; Mitosis; Ovariectomy; Phenols; Piperidines; Precipitin Tests; Proliferating Cell Nuclear Antigen; Receptors, Estrogen; Ribonucleases; RNA, Messenger; Signal Transduction; Tamoxifen; Thiophenes; Uterus	2000

Article

Year

Activation of a uterine insulin-like growth factor I signaling pathway by clinical and environmental estrogens: requirement of estrogen receptor-alpha.

Endocrinology, 2000, Volume: 141, Issue:9

Recent data indicate that insulin-like growth factor I (IGF-I) may have a function in mediating the mitogenic effects of 17beta-estradiol (E2) in the uterus and in regulating the growth of uterine neoplasms. This study was designed to determine whether synthetic and plant-derived chemicals that interact with estrogen receptor-alpha (ERalpha) and elicit estrogenic responses also mimic E2 by activating the uterine IGF-I signaling pathway. Ovariectomized adult female mice were treated with both environmental and clinically relevant chemicals previously reported to display estrogenic and/or antiestrogenic properties, and their uteri were evaluated for an activated IGF-I signaling pathway. Diethylstilbestrol, 4-hydroxytamoxifen, the raloxifene analog LY353381, 2,2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane (HPTE), bisphenol A, and genistein were shown to mimic E2 in the uterus by increasing the level of IGF-I messenger RNA, inducing IGF-I receptor (IGF-IR) tyrosine phosphorylation, stimulating the formation of IGF-IR signaling complexes, and increasing both proliferating cell nuclear antigen expression and the number of mitotic cells in the epithelium. The dose of chemical necessary to activate IGF-I signaling varied, with the order of potency: E2 = diethylstilbestrol > LY353381 > 4-hydroxytamoxifen > genistein > HPTE > bisphenol A. Administration of the chemicals to ERalpha knockout mice did not activate IGF-IR, indicating that ERalpha is required for activation of uterine IGF-IR by these diverse chemicals. This study demonstrates that several chemicals shown previously to display estrogenic activities also mimic E2 by activating uterine IGF-I signaling.

Topics: Animals; Benzhydryl Compounds; Blotting, Northern; Estradiol Congeners; Estrogen Antagonists; Estrogen Receptor alpha; Estrogens; Estrogens, Non-Steroidal; Female; Insulin-Like Growth Factor I; Mice; Mice, Knockout; Mitosis; Ovariectomy; Phenols; Piperidines; Precipitin Tests; Proliferating Cell Nuclear Antigen; Receptors, Estrogen; Ribonucleases; RNA, Messenger; Signal Transduction; Tamoxifen; Thiophenes; Uterus

2000