antiandrogens/inflammation

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In utero exposure to antiandrogens alters the responsiveness of the prostate to p,p'-DDE in adult rats and may induce prostatic inflammation.

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DDE is an environmental pollutant with antiandrogenic properties. Following administration to pregnant rats, DDE was shown to cause feminization in the male offspring at the neonatal stages but did not affect the pubertal growth of accessory sex organs. In this study, we examined the potential of in

Vascular and inflammatory effects of estrogen and anti-androgen therapy in the testis and epididymis of male to female transgender adults.

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The volume of ubiquitous chemicals with estrogenic properties is on the rise and some reports relate the increase in hormonal diseases to these compounds. A morphological and immunohistochemical analysis has been performed on 42 bilateral orchiectomy specimens from adult individuals who underwent

The antiandrogen cyproterone acetate induces synthesis of transforming growth factor beta 1 in the parenchymal cells of the liver accompanied by an enhanced sensitivity to undergo apoptosis and necrosis without inflammation.

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Recently, cases of liver damage and liver tumors have been reported after treatment of prostate cancer patients with the antiandrogen cyproterone acetate (CPA). In rat liver, CPA initiates a wave of DNA synthesis that is accompanied by apoptosis. In apoptotic hepatocytes, a latent form of

The story of spironolactones from 1957 to now: from sodium balance to inflammation.

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After the discovery of aldosterone (1953), many synthetic steroids were tested for their ability to block the sodium retaining and potassium excreting effect of synthetic mineralocorticoids in adrenalectomized rats. In the same years Kagawa discovered that 17-spirolactone steroids were effective to

Plasma monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha are increased in patients with polycystic ovary syndrome (PCOS) and associated with adiposity, but unaffected by pioglitazone treatment.

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OBJECTIVE Hirsutism is most often caused by polycystic ovary syndrome (PCOS). PCOS patients are characterized by insulin resistance, abdominal obesity and low-grade inflammation. Insulin sensitizing treatment reduces the inflammatory state, but the effect on serum levels of migration inhibitor

Influence of Testosterone on Inflammatory Response in Testicular Cells and Expression of Transcription Factor Foxp3 in T Cells.

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OBJECTIVE Previous studies demonstrated a strong association between low androgen levels and reduced capacity to mount an inflammatory response. However, the mechanisms underlying these observations are largely not understood. METHODS Generation of CD4+CD25+Foxp3+ regulatory T cells in Leydig

Oral contraceptive plus antiandrogen therapy and cardiometabolic risk in polycystic ovary syndrome.

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OBJECTIVE Oral contraceptives alone or in combination with antiandrogens are commonly used in the treatment for polycystic ovary syndrome (PCOS). We aimed to determine the effects of ethinyl estradiol/drospirenone (EE-DRSP) plus spironolactone therapy on inflammation and cardiometabolic risk in

Anti-androgen TSAA-291. III. Hormonal spectra of anti-androgen TSAA-291 (16 beta-ethyl-17 beta-hydroxy-4-oestren-3-one) and its derivatives.

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For the purpose of obtaining hormonal spectra of anti-androgen TSAA-291 and its derivatives, a variety of endocrine characteristics were studied. (1) Androgenic and anabolic activity : Subcutaneous administration of anti-androgen TSAA-291 and its acetate, TSAA-328, to the immature orchiectomized rat

[Treatment of acne with antiandrogens--an evidence-based review].

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BACKGROUND Increased sebaceous gland activity with seborrhea is one of the major pathogenetic factors in acne. Antiandrogen treatment targets the androgen-metabolizing follicular keratinocytes and the sebaceous gland leading to sebostasis, with a reduction of the sebum secretion rate of 12.5-65%.

Anti-androgen resistance in prostate cancer cells chronically induced by interleukin-1β.

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Chronic inflammation has been linked to cancer initiation and progression in a variety of tissues, yet the impact of acute and chronic inflammatory signaling on androgen receptor function has not been widely studied. In this report, we examine the impact of the inflammation-linked cytokine,

Effects of the antiandrogen, cyproterone acetate, on the induction of papillomas, DNA synthesis and ornithine decarboxylase activity in mouse skin.

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The antiandrogen, cyproterone acetate (CPA), applied simultaneously with 12-O-tetradecanoylphorbol-13-acetate (TPA) to the dorsal skin of male and female SENCAR mice initiated with 7,12-dimethylbenz[a]anthracene inhibited the production of papillomas of the skin. Although 125 and 250 micrograms of

Estrogens ameliorate remote organ inflammation induced by burn injury in rats.

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OBJECTIVE The present study was designed to investigate the role of sex steroids in burn-induced remote organ injury. METHODS Male Wistar albino rats were given burn trauma (n=39), and underwent castration or sham operation at 2 h following the burn injury. METHODS Rats were injected sc with either

Differential Impact of Insulin Sensitizers vs. Anti-Androgen on Serum Leptin Levels in Vitamin D Replete PCOS Women: A Six Month Open Labeled Randomized Study.

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Women with PCOS are linked to insulin resistance, inflammation, and vitamin D (VD) deficiency. The study endeavors to comprehend the differential impact of insulin sensitizers vs. anti-androgen on serum leptin levels among women with PCOS rendered vitamin D replete with high VD oral supplement. This

Functional, biochemical, and morphological hepatobiliary effects in rats chronically exposed to a steroidal antiandrogen.

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Yellow-brown deposits in intrahepatic bile ducts and portal macrophages were observed for male, but not female, Sprague- Dawley rats fed zanoterone, a steroidal antiandrogen, for >=3 months. The lesion did not affect biliary canaliculi and was associated with changes of biliary epithelium, portal

[Evaluation of anti-androgen therapy for benign prostatic hypertrophy by using transrectal prostatic ultrasonography].

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We evaluated the effect of anti-androgen therapy for benign prostatic hypertrophy on 33 patients who had undergone transrectal prostatic ultrasonography both before and after administration of anti-androgenic drugs in our clinic. Patients treated with chlormadinone acetate (CMA) orally, or TSAA-291

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