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The Stimulation of Steroid Biosynthesis by Luteinizing Hormone
Published in Mario Ascoli, Luteinizing Hormone Action and Receptors, 2019
Anita H. Payne, Patrick G. Quinn, John R. D. Stalvey
As in the immature male rat, the immature female rat had high gonadal 5α-reductase activity such that the major metabolite of progesterone was 5α-androstanediol.216,217 The 5α-androstanediol was probably formed via the 5α-pregnane pathway since the apparent Km of 5α-reductase is lower for progesterone than C19 steroids in the rat ovary.217,218 Following the first ovulation, 20α-hydroxprogesterone became the major metabolite and 5α-pregnanediol was formed to a lesser extent.219
Synthesis, Enzyme Localization, and Regulation of Neurosteroids
Published in Sheryl S. Smith, Neurosteroid Effects in the Central Nervous System, 2003
Evidence that acute exposure to AASs may have anxiolytic effects is provided by the study of Bing et al.81 in which male rats that received a single injection of testosterone before testing on Vogel’s conflict test accepted significantly more shocks than controls, consistent with an antianxiety action of testosterone. It is noteworthy that Bing et al.81 observe AAS-induced changes in anxiety within 24 h of a single injection of testosterone. First, it is unlikely that anything beyond physiological levels of testosterone would be present at 24 h after a single injection, given the rapid clearance of unesterified testosterone.4 However, if the anxiolytic effects were due to this testosterone treatment, then the narrow time frame, although not categorically excluding androgen receptor-dependent changes in gene expression, would be more consistent with a nongenomic mechanism of AAS action. Further evidence that androgens do indeed elicit rapid anxiolytic effects has been provided by a recent study that found that a single exposure to 500 yg of either testosterone, androsterone, or 3a-androstanediol reduced anxiety within 30 min.82 The anxiolytic effects of testosterone were blocked by co-injection of the GABAA receptor antagonists, bicuculline or picrotoxin, suggesting that the
Steroid Δ4-Reductases: their Physiological Role and Significance
Published in Ronald Hobkirk, Steroid Biochemistry, 1979
There have been a number of studies on androgen metabolism and levels in human prostate disease situations. Dihydrotestosterone contents for hypertrophic prostate (0.60 μ g/100 g) were higher than those for normal prostate (0.13 μ g/100 g); however, the rate of conversion of testosterone to 5α-dihydrotestosterone was similar for both types of tissue.117 In this first report,117 the 5α-dihydrotestosterone content was higher in the periurethral area of the gland when compared to the outer regions; prostatic hypertrophy begins in the periurethral area. 5α-Dihydrotestosterone administration to dogs did not consistently lead to prostatic hyperplasia; its further reduction product 5a-androstane-3↓,17β-diol did.118 This latter finding is interesting in view of the fact that prostatic androgen receptors bind 5α-dihydrotestosterone much more avidly than the androstanediol.
Updates on androgen replacement therapy and lower urinary tract symptoms: a narrative review
Published in The Aging Male, 2022
Raed M. Al-Zoubi, Mustafa Alwani, Omar M. Aboumarzouk, Mai Elaarag, Ahmad R. Al-Qudimat, Laxmi Ojha, Aksam Yassin
Even though several investigations were studied on the association between sex hormones and benign prostatic hyperplasia (BPH), few of them have reported the association between LUTS symptoms and circulating testosterone. Hypogonadism was observed in 20% of aging men with LUTS, but without any effect on the status of symptoms [7,13]. For instance, Litman et al. published a survey study on the possible association between testosterone and LUTS symptoms. Even though they reported good findings in terms of sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulphate (DHEAS), dihydrotestosterone (DHT), and oestradiol (E2), it was concluded that circulating levels of sex hormones are not significant predictors of urological symptoms and perhaps other factors control the pathophysiology of LUTS in hypogonadal men [14]. Furthermore, looking at LUTS and serum sex steroid hormones, there seems to be no associations between LUTS symptoms with total and calculated free testosterone, however, there seem to be some links with androstanediol glucuronide, a dihydrotestosterone metabolite, and estradiol [11].
Pharmacotherapeutic options for the treatment of menopausal symptoms
Published in Expert Opinion on Pharmacotherapy, 2021
Andrea R. Genazzani, Patrizia Monteleone, Andrea Giannini, Tommaso Simoncini
DHEA is most commonly administered orally as a nutritional supplement. After oral administration of 25–200 mg of DHEA, serum levels of DHEA and its sulfate ester, DHEAS, both peak in 2–4 hours, with the half-life of DHEA ranging from 5–12 hours in various studies [171]. DHEA is widely distributed in the human body, converted to the sex hormones in peripheral tissues, and can cross the blood-brain barrier. Most DHEA metabolites, glucuronide, sulfate conjugates, androsterone, and etiocholanolone, are eliminated in the urine within 24 hours. DHEA administered orally at 50 mg/day in healthy older individuals or patients with adrenal insufficiency produces circulating DHEA, DHEAS, androstanediol glucuronide, E1 E2 levels within the normal range in female and male young adults [172,173]. It is essential to keep in mind that, unlike testosterone, orally administered DHEA leads to an increase in estrogen activity, and therefore should not be administered in women with a history of breast cancer [174].
Applying a multiscale systems biology approach to study the effect of chronic low-dose exposure to uranium in rat kidneys
Published in International Journal of Radiation Biology, 2019
Stéphane Grison, Dimitri Kereselidze, David Cohen, Céline Gloaguen, Christelle Elie, Philippe Lestaevel, Audrey Legendre, Line Manens, Baninia Habchi, Mohamed Amine Benadjaoud, Georges Tarlet, Fabien Milliat, Jean-Charles Martin, Jean-Marc Lobaccaro, Maâmar Souidi
Putative annotation of the most discriminant features was performed with the freely accessible MZedDB database browser. The MS/MS spectra of some of these discriminative ions in biological samples were then compared with their authentic standard molecules to confirm the putative identification. Table 1 presents a list of the main discriminative markers identified in each of the three biological matrices. Palmitic acid, pentanoic acid, nicotinamide D-ribonucleotide, riboflavin-5-phosphate, phytosphingosine, prostaglandin F1 alpha, 2-lysolecithin, glycochenodeoxycholate 7-sulfate, linoleic acid, oleic acid, 25-Hydroxyvitamin D3, and palmitoleoyl-ethanolamide were identified in kidney tissue. Docosatetraenoyl ethanolamide, arachidonylethanolamide, dihomo-gamma-linolenoyl ethanolamide, androstanediol, and 7a-hydroxyandrost-4-ene-3,17-dione were identified in plasma. Finally, N1-methyl-2-pyridone-5-carboxamide, 4-hydroxyphenylacetylglycine, 4-pyridoxic acid, lysophosphatidylcholine (LysoPc 16:0), creatine, and N1-methylnicotinamide were found in urine.