antiandrogens/ذرة

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An environmental antiandrogen, vinclozolin, alters the organization of play behavior.

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During mammalian sexual differentiation, the androgens, testosterone and dihydrotestosterone are critical for the organization of the male phenotype. In rats, play behavior is sexually dimorphic. Administration of exogenous androgens during the perinatal period results in masculine-like play

Antiandrogen flutamide affects folliculogenesis during fetal development in pigs.

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Androgen deficiency during prenatal development may affect the expression of genes involved in the folliculogenesis regulation. In order to study the effect of antiandrogen on fetal ovarian development, pregnant gilts were injected with flutamide (for 7 days, 50 mg/kg bodyweight per day) or corn oil

A transcriptome approach evaluating effects of neonatal androgen and anti-androgen treatments on regulation of luteal function in sexually mature pigs.

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The current study was designed to gain insights into regulatory mechanisms mediating long-term effects of androgen excess or deficiency on corpus luteum function in pigs. Piglets were injected subcutaneously with testosterone propionate (TP, an androgen), flutamide (FLU, an anti-androgen) or corn

Androgens and environmental antiandrogens affect reproductive development and play behavior in the Sprague-Dawley rat.

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In mammals, exposure to androgens early in development is essential for masculinization of the male reproductive phenotype. Male fetuses exposed to antiandrogens during perinatal life are permanently demasculinized in their morphology and physiology, whereas exposure to exogenous androgens

The impact of antiandrogen flutamide on the hypoxia inducible factor 1α and vascular endothelial growth factor A gene and protein expression in the pig placenta during late pregnancy.

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BACKGROUND In contrast to estradiol action, little is known about androgen signaling in placental development. The purpose of this study was to evaluate the impact of diminished androgen action on hypoxia inducible factor 1a (HIF-1a) and vascular endothelial growth factor A (VEGFA) protein

Developmental effects of an environmental antiandrogen: the fungicide vinclozolin alters sex differentiation of the male rat.

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In humans and rodents, exposure to hormonally active chemicals during sex differentiation can produce a wide range of abnormal sexual phenotypes including masculinized and defeminized females and feminized and demasculinized males. Although numerous "environmental estrogens," including pesticides,

Organizational effects of the antiandrogen, vinclozolin, on penis development in the mouse.

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Endocrine disrupting chemicals (EDCs) are pollutants found throughout the environment that disrupt normal endocrine processes. In mice, penis development is thought to be most susceptible to EDCs during a critical developmental window occurring on embryonic days (E) 15.5-17.5. However, androgen

A mixture of the "antiandrogens" linuron and butyl benzyl phthalate alters sexual differentiation of the male rat in a cumulative fashion.

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Prenatal exposure to environmental chemicals that interfere with the androgen signaling pathway can cause permanent adverse effects on reproductive development in male rats. The objectives of this study were to 1) determine whether a documented antiandrogen butyl benzyl phthalate (BBP) and/or

Pharmacokinetics and dosimetry of the antiandrogen vinclozolin after oral administration in the rat.

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Vinclozolin (V) is a fungicide with antiandrogenic properties. To determine the pharmacokinetics and dosimetry of V, adult male rats were administered an oral dose of V (100 mg/kg) in corn oil and sacrificed over time after dosing. V and its metabolites were analyzed in serum and tissues by high

Altered gene expression during rat Wolffian duct development in response to in utero exposure to the antiandrogen linuron.

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Linuron is an herbicide with weak androgen receptor (AR) antagonist activity. Exposure to linuron from gestation days (GD) 12 to 21 perturbs androgen-dependent male reproductive development. In utero exposure to 50-mg/kg/day linuron induces malformations of the epididymis and the vas deferens. The

Lactational Exposure to Di (2-ethylhexyl) Phthalate Impairs the Ovarian and Uterine Function of Adult Offspring Rat.

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Phthalates, a class of chemicals used as plasticizers, are economically important due to several industrial applications. Di-(2-ethylhexyl) phthalate (DEHP) is the most commonly used phthalate plasticizer, and it has been described as a potent antiandrogen in males. In this study, lactating dams

Effects of perinatal exposure to flutamide on sex hormone responsiveness in F1 male rats.

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Pregnant rats were administered flutamide (0 and 10 mg/kg, p.o.) from gestation Day 14 to post-parturition Day 3 and effects on responsiveness to androgens (testosterone propionate, TP; dihydrotestosterone, DHT) in male offspring were examined with a Hershberger assay. Male pups of each group were

Preliminary investigation of changes in the sexually dimorphic nucleus of the rat medial preoptic area following prenatal exposure to fenitrothion.

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In vitro, the organophosphate insecticide fenitrothion is a potent competitive androgen receptor antagonist, whereas in vivo it affects the development of the male rat reproductive system. The purpose of this pilot study was to determine whether prenatal exposure to fenitrothion affects development

Neonatal Exposure to Agonists and Antagonists of Sex Steroid Receptors Affects AMH and FSH Plasma Level and Their Receptors Expression in the Adult Pig Ovary.

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In this study piglets were injected with testosterone propionate (TP, an androgen), flutamide (FLU, an antiandrogen), 4-tert-octylphenol (OP, an estrogenic compound), ICI 182,780 (ICI, an antiestrogen) or corn oil (controls) between postnatal days 1 and 10 (N = 5/group). Then plasma

[Effects of Di (2-ethylhexyl) phthalate on the testis and testicular gubernaculum of fetal KM mice].

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OBJECTIVE To explore the effects of Di (2-ethylhexyl) phthalate (DEHP) on the testis and testicular gubernaculum of fetal KM mice in vivo and to investigate the mechanism of DEHP-induced cryptorchidism. METHODS Thirty healthy pregnant KM mice were randomly and equally divided into a blank control

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