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Urological Anti-cancer Agents
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Bernadett Szabados, Thomas Powles
Abiraterone acetateSelective and irreversible blockage of 17α-hydroxylase and C17,20 lyase.Inhibition of androstenedione synthesis in the testes and adrenal glands.Decreased systemic levels of testosterone and cortisol.Increased levels of mineralocorticoid steroidsUsed in combination with prednisone/prednisolone to prevent drug-induced hyperaldosteronism (high sodium, low potassium).Side effects: hypertension, hypokalaemia, increased transaminase levels.Current uses:Castration-sensitive metastatic prostate cancer combined with ADT.Castration-resistant prostate cancer (CRPC) in chemotherapy − naïve and pre-treated setting.
Adrenocortical Disease
Published in T.M. Craft, P.M. Upton, Key Topics In Anaesthesia, 2021
The adrenal cortex produces glucocorticoid, mineralocorticoid and sex hormones (mainly testosterone). Cortisol, the principal glucocorticoid, modulates stress and inflammatory responses. It is a potent stimulator of gluconeogenesis and antagonizes insulin. Aldosterone is the principal mineralocorticoid. It causes increased sodium reabsorption, and potassium and hydrogen ion loss at the distal renal tubule. Adrenal androgen production increases markedly at puberty, declining with age thereafter. Androstenedione is converted by the liver to testosterone in the male and oestrogen in the female. Cortisol and androgen production are under diurnal pituitary control (adrenocorticotrophic hormone — ACTH). Aldosterone is released in response to angiotensin II, produced following renal renin release and subsequent pulmonary angiotensin I conversion.
Sex Hormones in Autoimmunity
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
Elizabeth S. Raveche, Alfred D. Steinberg
The ovaries in females are the main source for estrogens. The testes in males may account for as much as 30% of the estrogen. Peripheral conversion of androgens to estrogens is also very important in the production of estrogen. A significant fraction of androstenedione is converted to estrone. The androstenedione in premenopausal females is derived about equally from the ovaries and the adrenal glands. Following menopause, the ovarian production of androstenedione falls off, but the adrenal gland secretion continues. The conversion of androstenedione to estrone is approximately 1% in lean premenopausal women and rises to 2 to 3% in postmenopausal women. A number of conditions increase the production of estrone from circulating androstenedione, such as aging and obesity. Several studies have suggested that most extraglandular estrogen formation occurs in adipose tissue.
The vagina as source and target of androgens: implications for treatment of GSM/VVA, including DHEA
Published in Climacteric, 2023
S. Cipriani, E. Maseroli, S. A. Ravelli, L. Vignozzi
As a steroid prohormone and an intermediate in the synthetic pathway of androgens and estrogens, androstenedione could theoretically represent a therapeutic strategy against GSM. It can be administered as an oral formulation; however, scarce evidence is available regarding its safety and its impact on sexual function. In a small study published in 2002, 30 healthy postmenopausal women randomly took a single oral dose of 50 mg or 100 mg androstenedione or placebo [53]. The authors concluded that both androstenedione doses were able to significantly increase testosterone and estrone, but not estradiol serum levels in the treated groups, with peak testosterone levels higher than the normal upper limit in 4/10 patients in the 50 mg group and 6/10 in the 100 mg group [53]. Consequently, longer-term data, safety and efficacy profiles of androstenedione treatment are needed.
Treatment of copper nanoparticles (CuNPs) for two spermatogenic cycles impairs testicular activity via down-regulating steroid receptors and inhibition of germ cell proliferation in a mice model
Published in Nanotoxicology, 2022
Vanrohlu Nicy, Milirani Das, Guruswami Gurusubramanian, Pradip Mondal, Vikas Kumar Roy
The serum androstenedione, testosterone, estradiol and progesterone level were assayed using human ELISA kit (Androstenedione Cat# DKO008, DiaMetra, Italy. Testosterone Cat# DKO002, Diametra, Italy, Estradiol Cat# DKO003, DiaMedia, Italy, Progesterone Cat# DKO006, DiaMetra, India). The lowest detectable concentration of estradiol that could be distinguished from the calibrator zero is 8.68 pg/mL at the 95% confidence limit. The within assay variability was ≤9% and the between assay variability was ≤10% for estrogen. The lowest detectable concentration of testosterone that could be distinguished from calibrator 0 is 0.10 ng/mL at the 95% confidence level. The within assay variability was ≤7.0% and the between assay variability was ≤8.3% for testosterone. The lowest detectable concentration of progesterone that could be distinguished from calibrator 0 is 0.05 ng/mL at the 95% confidence limit. The within assay variability was ≤4% and the between assay variability was ≤9.3% for progesterone. Intra assay variation and intra-assay variations were 10.0% and ≤ 9.3% for androstenedione.
Testosterone use in postmenopausal women
Published in Climacteric, 2021
A. Martínez-García, S. R. Davis
In premenopausal women, circulating testosterone is directly from ovarian production, as well as being derived from precursor hormones secreted by the ovaries and adrenal glands. These precursors include dehydroepiandrosterone (DHEA) and DHEA sulfate, with the latter almost entirely of adrenal origin, and androstenedione which is secreted by both the adrenals and ovaries. It has been estimated that the ovaries and adrenals each contribute 50% to the circulating testosterone pool during the premenopausal period8,9. The testosterone precursors exhibit little biological activity. After their secretion into the circulation, they are activated in peripheral target tissues, mainly adipose tissue and skin, by local intracellular steroidogenic enzymes. Androstenedione, which is also produced peripherally from DHEA, is further metabolized in target tissues to testosterone or estrone10. In turn, testosterone may be converted to dihydrotestosterone, the most potent androgen, or to estradiol within the cells. These biosynthetic pathways in peripheral target tissues are the main source of estrogen and testosterone production in postmenopausal women11.