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Y Ohno - One of the best experts on this subject based on the ideXlab platform.
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Modulation by estrogens and xenoestrogens of recombinant human neuronal nicotinic receptors.
European journal of pharmacology, 2001Co-Authors: K Nakazawa, Y OhnoAbstract:The effects of estrogens and xenoestrogens on human neuronal nicotinic acetylcholine receptor/channels were examined by expressing recombinant channels in Xenopus oocytes. When functional channels were expressed with alpha3 and beta4 subunits, estrogens (17beta-estradiol, 17alpha-estradiol, 17alpha-ethynylestradiol and Diethylstilbestrol) and xenoestrogens (bisphenol A, p-nonylphenol and p-octylphenol) inhibited an ionic current activated by acetylcholine at concentrations up to 100 microM. When the subunit combination was changed to alpha4beta2, diethystilbestrol and the xenoestrogens inhibited the acetylcholine-activated current, but 17beta-estradiol or 17alpha-estradiol did not. For 17alpha-ethynylestradiol, the current through the alpha4beta2 receptor/channel was inhibited at 1 microM, but it was markedly enhanced at 10 and 100 microM. Tamoxifen (10 microM), an antiestrogen, itself inhibited the acetylcholine-activated current but did not antagonize the current modulations induced by the estrogens and the xenoestrogens. These and additional results suggest that human neuronal nicotinic acetylcholine receptors are the targets of non-genomic actions of estrogens and xenoestrogens.
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Modulation by estrogens and xenoestrogens of recombinant human neuronal nicotinic receptors.
European Journal of Pharmacology, 2001Co-Authors: K Nakazawa, Y OhnoAbstract:The effects of estrogens and xenoestrogens on human neuronal nicotinic acetylcholine receptor/channels were examined by expressing recombinant channels in Xenopus oocytes. When functional channels were expressed with α3 and β4 subunits, estrogens (17β-estradiol, 17α-estradiol, 17α-ethynylestradiol and Diethylstilbestrol) and xenoestrogens (bisphenol A, p-nonylphenol and p-octylphenol) inhibited an ionic current activated by acetylcholine at concentrations up to 100 μM. When the subunit combination was changed to α4β2, diethystilbestrol and the xenoestrogens inhibited the acetylcholine-activated current, but 17β-estradiol or 17α-estradiol did not. For 17α-ethynylestradiol, the current through the α4β2 receptor/channel was inhibited at 1 μM, but it was markedly enhanced at 10 and 100 μM. Tamoxifen (10 μM), an antiestrogen, itself inhibited the acetylcholine-activated current but did not antagonize the current modulations induced by the estrogens and the xenoestrogens. These and additional results suggest that human neuronal nicotinic acetylcholine receptors are the targets of non-genomic actions of estrogens and xenoestrogens.
Fujio Kayama - One of the best experts on this subject based on the ideXlab platform.
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Suppression of erythropoietin induction by Diethylstilbestrol in rats
Archives of toxicology, 2013Co-Authors: Hyogo Horiguchi, Etsuko Oguma, Takako Sakamoto, Katsuyuki Murata, Fujio KayamaAbstract:Diethylstilbestrol is an estrogenic endocrine disrupter that has diverse health effects in humans. Bisphenol A is another estrogen-like chemical with possible similar effects to Diethylstilbestrol, which has been increasingly used for industry to lead to globally widespread human exposure to it. Hematopoiesis is another of their possible targets, since estrogen suppresses erythropoietin induction to induce anemia. The aim of this study was to clarify the effects of Diethylstilbestrol and bisphenol A on erythropoietin induction in rats. We observed the effects of one-shot subcutaneous injection of Diethylstilbestrol or bisphenol A on hypoxia-, bleeding-, and cobalt-stimulated erythropoietin induction within 24 h and the hematological outcomes after repeated subcutaneous injection of Diethylstilbestrol three times a week for 1 month in rats. Diethylstilbestrol at 10–1,000 μg/kg suppressed stimulus-elevated levels of plasma erythropoietin and its renal mRNA induction. In contrast, bisphenol A at 1,000 μg/kg did not suppress plasma erythropoietin elevated by any stimuli. Repeated injection of Diethylstilbestrol at 1,000 μg/kg to rats for 1 month induced an anemic trend due to decelerated erythropoiesis through the insufficient production of erythropoietin, mimicking the effects of estradiol. In conclusion, Diethylstilbestrol has a suppressive effect on erythropoietin induction, leading to deceleration of erythropoiesis and the development of anemia.
Arthur L. Herbst - One of the best experts on this subject based on the ideXlab platform.
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Infertility among Women Exposed Prenatally to Diethylstilbestrol
American journal of epidemiology, 2001Co-Authors: Julie R. Palmer, Elizabeth E. Hatch, R. Sowmya Rao, Raymond H. Kaufman, Arthur L. Herbst, Kenneth L. Noller, Linda Titus-ernstoff, Robert N. HooverAbstract:Although it is well established that women exposed to Diethylstilbestrol in utero have an increased risk of spontaneous abortion, ectopic pregnancy, and preterm delivery, it is not known whether they also have an increased risk of infertility. The authors assessed this question in data from a collaborative follow-up study of the offspring of women who took Diethylstilbestrol during pregnancy. In 1994, 1,753 Diethylstilbestrol-exposed and 1,050 unexposed women from an ongoing cohort study (National Cooperative Diethylstilbestrol Adenosis Study and Dieckmann cohorts) provided data on difficulties in conceiving and reasons for the difficulty. Age-adjusted relative risks were computed for the association of Diethylstilbestrol exposure with specific types of infertility. A greater proportion of exposed than unexposed women were nulligravid (relative risk (RR) = 1.3, 95% confidence interval (CI): 1.1, 1.5), and a greater proportion had tried to become pregnant for at least 12 months without success (RR = 1.8, 95% CI: 1.6, 2.1). Diethylstilbestrol exposure was significantly associated with infertility due to uterine and tubal problems, with relative risks of 7.7 (95% CI: 2.3, 25) and 2.4 (95% CI: 1.2, 4.6), respectively. The present findings indicate that Diethylstilbestrol-exposed women have a higher risk of infertility than do unexposed women and that the increased risk of infertility is primarily due to uterine or tubal problems.
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Fertility in men exposed prenatally to Diethylstilbestrol.
The New England journal of medicine, 1995Co-Authors: Allen J. Wilcox, Paige P. Hornsby, Clarice R. Weinberg, Donna D. Baird, Arthur L. HerbstAbstract:Background Prenatal exposure to Diethylstilbestrol causes infertility in male mice and has been associated with malformations of the genital tract in men. However, little is known about the fertility of men who have been exposed prenatally to Diethylstilbestrol. Methods In 1950 through 1952, 1646 pregnant women were enrolled in a randomized, placebo-controlled clinical trial of Diethylstilbestrol at Chicago Lying-in Hospital. We interviewed men who were born to the women during that study about their fertility. Results Four decades after their birth, we were able to trace 548 of the surviving sons (68 percent). Ninety percent consented to be interviewed (253 who had been exposed to Diethylstilbestrol in utero and 241 who had not been exposed). Congenital malformations of the genitalia were reported three times as often by the Diethylstilbestrol-exposed men as by the sons of the women in the placebo group. Within the exposed group, malformations were reported twice as often among those exposed to diethylst...
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Effects on the menstrual cycle of in utero exposure to Diethylstilbestrol.
American journal of obstetrics and gynecology, 1994Co-Authors: Paige P. Hornsby, Allen J. Wilcox, Clarice R. Weinberg, Arthur L. HerbstAbstract:Abstract OBJECTIVES: The purpose of this study was to determine the effects of in utero exposure to Diethylstilbestrol on the menstrual cycle. STUDY DESIGN: This was a prospective cohort study of 198 Diethylstilbestrol-exposed women and 162 unexposed controls, recruited from women whose mothers participated in a randomized trial of Diethylstilbestrol in pregnancy at the Chicago Lying-In Hospital from 1950 to 1952. Women with severe menstrual abnormality were excluded from the study. RESULTS: Diethylstilbestrol exposure was associated with a statistically significantly decreased duration of menstrual bleeding of approximately one half day and a lower average daily bleeding score (self-reported). We found no evidence for effects of Diethylstilbestrol exposure on cycle length or variability of cycle length. Exposure was not related to symptoms of dysmenorrhea. CONCLUSIONS: The decreased duration and amount of menstrual bleeding among Diethylstilbestrol-exposed women could be due to direct effects on the uterus. The lack of an effect on cycle length and variability appears to indicate that endocrine function is not grossly disturbed in those women studied. (AM J OBSTET GYNECOL 1994;170:709-15.)
K Nakazawa - One of the best experts on this subject based on the ideXlab platform.
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Modulation by estrogens and xenoestrogens of recombinant human neuronal nicotinic receptors.
European journal of pharmacology, 2001Co-Authors: K Nakazawa, Y OhnoAbstract:The effects of estrogens and xenoestrogens on human neuronal nicotinic acetylcholine receptor/channels were examined by expressing recombinant channels in Xenopus oocytes. When functional channels were expressed with alpha3 and beta4 subunits, estrogens (17beta-estradiol, 17alpha-estradiol, 17alpha-ethynylestradiol and Diethylstilbestrol) and xenoestrogens (bisphenol A, p-nonylphenol and p-octylphenol) inhibited an ionic current activated by acetylcholine at concentrations up to 100 microM. When the subunit combination was changed to alpha4beta2, diethystilbestrol and the xenoestrogens inhibited the acetylcholine-activated current, but 17beta-estradiol or 17alpha-estradiol did not. For 17alpha-ethynylestradiol, the current through the alpha4beta2 receptor/channel was inhibited at 1 microM, but it was markedly enhanced at 10 and 100 microM. Tamoxifen (10 microM), an antiestrogen, itself inhibited the acetylcholine-activated current but did not antagonize the current modulations induced by the estrogens and the xenoestrogens. These and additional results suggest that human neuronal nicotinic acetylcholine receptors are the targets of non-genomic actions of estrogens and xenoestrogens.
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Modulation by estrogens and xenoestrogens of recombinant human neuronal nicotinic receptors.
European Journal of Pharmacology, 2001Co-Authors: K Nakazawa, Y OhnoAbstract:The effects of estrogens and xenoestrogens on human neuronal nicotinic acetylcholine receptor/channels were examined by expressing recombinant channels in Xenopus oocytes. When functional channels were expressed with α3 and β4 subunits, estrogens (17β-estradiol, 17α-estradiol, 17α-ethynylestradiol and Diethylstilbestrol) and xenoestrogens (bisphenol A, p-nonylphenol and p-octylphenol) inhibited an ionic current activated by acetylcholine at concentrations up to 100 μM. When the subunit combination was changed to α4β2, diethystilbestrol and the xenoestrogens inhibited the acetylcholine-activated current, but 17β-estradiol or 17α-estradiol did not. For 17α-ethynylestradiol, the current through the α4β2 receptor/channel was inhibited at 1 μM, but it was markedly enhanced at 10 and 100 μM. Tamoxifen (10 μM), an antiestrogen, itself inhibited the acetylcholine-activated current but did not antagonize the current modulations induced by the estrogens and the xenoestrogens. These and additional results suggest that human neuronal nicotinic acetylcholine receptors are the targets of non-genomic actions of estrogens and xenoestrogens.
Hiroshi Yokota - One of the best experts on this subject based on the ideXlab platform.
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adrenal steroidogenesis disruption caused by hdl cholesterol suppression in Diethylstilbestrol treated adult male rat
Endocrine, 2016Co-Authors: Satoko Haeno, Kousuke Yamaguchi, Michiko Sato, Naoyuki Maeda, Hiroshi YokotaAbstract:The synthetic estrogen Diethylstilbestrol is used to prevent miscarriages and as a therapeutic treatment for prostate cancer, but it has been reported to have adverse effects on endocrine homeostasis. However, the toxicity mechanism is poorly understood. Recently, we reported that Diethylstilbestrol impairs adrenal steroidogenesis via cholesterol insufficiency in adult male rats. In the present study, we found that the adrenal cholesterol level was significantly reduced without of the decrease in other precursors in the adrenal steroidogenesis 24 h after a single dose of Diethylstilbestrol (0.33 μg/g body mass). The serum HDL/cholesterol level was also reduced only 12 h after the Diethylstilbestrol exposure. The level of Apo E, which is indispensable for HDL/cholesterol maturation, was decreased in both the HDL and VLDL/LDL fractions, whereas the level of Apo A1, which is an essential constituent of HDL, was not altered in the HDL fraction. Because the liver is a major source of Apo E and Apo A1, the secretion rates of these proteins were examined using a liver perfusion experiment. The secretion rate of Apo A1 from the liver was consistent between DES-treated and control rats, but that of Apo E was comparatively suppressed in the DES-treated rats. The disruption of adrenal steroidogenesis by Diethylstilbestrol was caused by a decrease in serum HDL/cholesterol, which is the main source of adrenal steroidogenesis, due to the inhibition of Apo E secretion from the liver.