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1
Ziegenfuss, Tim N., John M. Berardi, Lonnie M. Lowery, and Jose Antonio. "Effects of Prohormone Supplementation in Humans: A Review." Canadian Journal of Applied Physiology 27, no. 6 (December 1, 2002): 628–45. http://dx.doi.org/10.1139/h02-037.
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Despite a relative dearth of information on their effects, supplementation with prohormones has become a popular practice. Unlike synthetic anabolic-androgenic steroids, many of these over-the-counter androgens are produced endogenously by adrenal, gonadal and peripheral steroidogenic pathways as part of the normal sexual and reproductive hormonal milieu. It has been contended that peripheral enzymatic conversion of these prohormones to testosterone or nortestosterone (via ingestion of androstenedione/androstenediol or 19-nor-androstenedione/androstenediol, respectively) might lead to anabolic and/or ergogenic effects. Existing data suggest that acute oral ingestion of >= 200 mg androstenedione or androstenediol modestly and transiently increases serum testosterone concentrations in men; however, this is accompanied by greater increases in circulating estrogen(s). At doses < 300 mg/d, oral supplementation for as long as 12-weeks with androstenedione or androstenediol has no effect on body composition or physical performance and decreases high-density lipoprotein cholesterol. Similarly, oral supplementation with norandrostenedione and norandrostenediol for up to eight weeks has no effect on body composition or physical performance. In light of these data, new products have been developed that use alternative modes of prohormone administration (sublingual/transbuccal and cyclodextrin-complexation). Future studies should critically examine the effects of these approaches. However, within the framework of the research reviewed, over-the-counter oral prohormone supplementation is ineffective at increasing muscle mass or athletic performance. As a result of the potential health concerns that have been raised, the risk to benefit ratio of using these substances orally seems unfavorable. Keywords: androstenediol, androstenedione, norandrostenedione, norandrostenediol, ergogenic aid
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Gwartney, Daniel L., and Jeffrey R. Stout. "Androstenedione." Strength and Conditioning Journal 21, no. 1 (February 1999): 65. http://dx.doi.org/10.1519/00126548-199902000-00016.
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Dlugovitzky, Diana G., María Sol Fontela, Diego J. Martinel Lamas, Ricardo A. Valdez, and Marta C. Romano. "Mycobacterium smegmatis synthesizes in vitro androgens and estrogens from different steroid precursors." Canadian Journal of Microbiology 61, no. 7 (July 2015): 451–55. http://dx.doi.org/10.1139/cjm-2015-0025.
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Fast-growing mycobacteria such as Mycobacterium sp. and Mycobacterium smegmatis degrade natural sterols. They are a model to study tuberculosis. Interestingly, M. smegmatis has been found in river effluents derived from paper production, and therefore, it would be important to gain further insight into its capacity to synthesize steroids that are potential endocrine disruptors affecting the development and reproduction of fishes. To our knowledge, the capacity of M. smegmatis to synthesize estrogens and even testosterone has not been previously reported. Therefore, the objective of this study was to investigate the capacity of M. smegmatis to synthesize in vitro testosterone and estrogens from tritiated precursors and to investigate the metabolic pathways involved. Results obtained by thin-layer chromatography showed that 3H-progesterone was transformed to 17OH-progesterone, androstenedione, testosterone, estrone, and estradiol after 6, 12, or 24 h of incubation. 3H-androstenedione was transformed into testosterone and estrogens, mainly estrone, and 3H-testosterone was transformed to estrone and androstenedione. Incubation with 3H-dehydroepiandrosterone rendered androstenediol, testosterone, and estrogens. This ability to transform less potent sex steroids like androstenedione and estrone into other more active steroids like testosterone and estradiol or vice versa suggests that M. smegmatis can influence the amount of self-synthesized strong androgens and estrogens and can transform those found in the environment.
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Broeder, Craig E. "Oral Andro-Related Prohormone Supplementation: Do the Potential Risks Outweigh the Benefits?" Canadian Journal of Applied Physiology 28, no. 1 (February 1, 2003): 102–16. http://dx.doi.org/10.1139/h03-009.
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Androstenedione, 4-androstenediol, 5-androstenediol, 19-norandrostenediol and 19-norandrostenedione are commonly referred to as "Andro" prohormones. Over the last few years, supplementation using these prohormones has been aggressively marketed to the general public. Supplement manufacturers often claim that Andro use improves serum testosterone concentrations, increases muscular strength and muscle mass, helps to reduce body fatness, enhances mood, and improves sexual performance. However, to date, most studies contradict these claims. In contrast, several studies using oral Andro related prohormones show that Andro use can abnormally elevate estrogen related hormones as well as alterations in hormonal markers (i.e., abnormal elevations in serum estrogen) thought to increase a person's risk for developing prostate or pancreatic cancers. In addition, most studies also indicate that significant declines in high-density lipoproteins occur leading to an increased cardiovascular disease risk. Thus, to date, the current research base suggests that Andro prohormone use does not support manufacturer claims. But it does suggest there should be strong concerns regarding long-term oral Andro prohormone use, especially regarding its effects on blood lipids and estrogen hormone profiles. Key words: resistance exercise, androstenedione, androstenediol, anti-aging
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Brown, Gregory A., Emily R. Martini, B. Scott Roberts, Matthew D. Vukovich, and Douglas S. King. "Acute hormonal response to sublingual androstenediol intake in young men." Journal of Applied Physiology 92, no. 1 (January 1, 2002): 142–46. http://dx.doi.org/10.1152/jappl.2002.92.1.142.
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The effectiveness of orally ingested androstenediol in raising serum testosterone concentrations may be limited because of hepatic breakdown of the ingested androgens. Because androstenediol administered sublingually with cyclodextrin bypasses first-pass hepatic catabolism, we evaluated the acute hormonal response to sublingual cyclodextrin androstenediol supplement in young men. Eight men (22.9 ± 1.2 yr) experienced in strength training consumed either 20 mg androstenediol in a sublingual cyclodextrin tablet (Sl Diol) or placebo (Pl) separated by at least 1 wk in a randomized, double-blind, crossover manner. Blood samples were collected before supplementation and at 30-min intervals for 3 h after supplementation. Serum hormone concentrations did not change with Pl. Serum androstenedione concentrations were increased ( P < 0.05) above baseline (11.2 ± 1.1 nmol/l) with Sl Diol from 60 to 180 min after intake and reached a peak concentration of 25.2 ± 2.9 nmol/l at 120 min. Serum free testosterone concentrations were increased from 86.2 ± 9.1 pmol/l with Sl Diol from 30 to 180 min and reached a peak concentration of 175.4 ± 12.2 pmol/l at 60 min. Serum total testosterone concentrations increased above basal (25.6 ± 2.3 nmol/l) from 30 to 180 min with Sl Diol and reached a peak concentration of 47.9 + 2.9 nmol/l at 60 min. Serum estradiol concentrations were elevated ( P < 0.05) above baseline (0.08 ± 0.01 nmol/l) from 30 to 180 min with Sl Diol and reached 0.14 ± 0.02 nmol/l at 180 min. These data indicate that sublingual cyclodextrin androstenediol intake increases serum androstenedione, free testosterone, total testosterone, and estradiol concentrations.
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Rasmussen, Blake B., Elena Volpi, Dennis C. Gore, and Robert R. Wolfe. "Androstenedione Does Not Stimulate Muscle Protein Anabolism in Young Healthy Men1." Journal of Clinical Endocrinology & Metabolism 85, no. 1 (January 1, 2000): 55–59. http://dx.doi.org/10.1210/jcem.85.1.6322.
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Androstenedione is the immediate precursor of testosterone. Androstenedione intake has been speculated to increase plasma testosterone levels and muscle anabolism. Thus, androstenedione supplements have become widely popular in the sport community to improve performance. This study was designed to determine whether 5 days of oral androstenedione (100 mg/day) supplementation increases skeletal muscle anabolism. Six healthy young men were studied before the treatment period and after 5 days of oral androstenedione supplementation. Muscle protein turnover parameters were compared to those of a control group studied twice as well and receiving no treatment. We measured muscle protein kinetics using a three-compartment model involving infusion of l-[ring-2H5]phenylalanine, blood sampling from femoral artery and vein, and muscle biopsies. Plasma testosterone, androstenedione, LH, and estradiol concentrations were determined by RIA. After ingestion of oral androstenedione, plasma testosterone and LH concentrations did not change from basal, whereas plasma androstenedione and estradiol concentrations were significantly increased (P < 0.05). Compared to a control group, androstenedione did not affect muscle protein synthesis and breakdown, or phenylalanine net balance across the leg. We conclude that oral androstenedione does not increase plasma testosterone concentrations and has no anabolic effect on muscle protein metabolism in young eugonadal men.
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Lea, CK, V. Moxham, MJ Reed, and AM Flanagan. "Androstenedione treatment reduces loss of cancellous bone volume in ovariectomised rats in a dose-responsive manner and the effect is not mediated by oestrogen." Journal of Endocrinology 156, no. 2 (February 1, 1998): 331–39. http://dx.doi.org/10.1677/joe.0.1560331.
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We have tested the hypothesis that androstenedione (administered as 21-day, slow-release pellets) is converted to active sex steroids and reduces bone turnover in the ovariectomised rat model. We found that ovariectomy resulted in a minor but significant reduction in plasma concentrations of androstenedione and testosterone and a more significant reduction in oestrone (E1) and oestradiol (E2). This was associated with the expected substantial loss of metaphyseal cancellous bone volume. Androstenedione (1.5-100 mg) pellets increased the plasma concentrations of androstenedione and testosterone above those in the ovariectomised (ovx) rats in a dose-responsive manner, whereas E2 plasma concentrations were increased to a minor but significant degree above those in the ovx animals. Androstenedione reduced loss of cancellous bone volume in a dose-dependent fashion by reducing bone turnover. The 1.5, 5 and 100 mg androstenedione-induced effect on bone turnover was not abrogated by simultaneous treatment with Arimidex, an aromatase inhibitor. This implies that the skeletal-protective effect of androstenedione was not oestrogen-mediated.
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Doggui, Radhouene. "Immunoanalytical profile of androstenedione." Annales de biologie clinique 74, no. 4 (July 2016): 495–502. http://dx.doi.org/10.1684/abc.2016.1171.
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&NA;. "Beware of androstenedione contamination." Inpharma Weekly &NA;, no. 1266 (December 2000): 19. http://dx.doi.org/10.2165/00128413-200012660-00049.
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Thomson, S., A. M. Wallace, and B. Cook. "A 125I-radioimmunoassay for measuring androstenedione in serum and in blood-spot samples from neonates." Clinical Chemistry 35, no. 8 (August 1, 1989): 1706–12. http://dx.doi.org/10.1093/clinchem/35.8.1706.
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Abstract We developed a radioimmunoassay with a gamma-emitting radioligand to measure androstenedione in human serum and in dried blood-spot samples from newborns. Antisera were raised in rabbits against androstenedione linked to bovine serum albumin at positions 3, 6, or 11 on the steroid nucleus. Radioligands were prepared by linking [125I]iodohistamine at positions 3, 6, or 11. Linkages were through either carboxymethyloxime or hemisuccinate bridges. All label and antibody combinations were examined, and the most sensitive and specific combination (antiserum raised against androstenedione-3-carboxymethyloxime-bovine serum albumin with an androstenedione-carboxymethyloxime-[125I]iodohistamine label) was selected for full evaluation. We report the performance of these selected reagents in an immunoassay for androstenedione in both serum and dried blood-spot samples from neonates. We measured concentrations of androstenedione in serum under normal and pathological conditions such as congenital adrenal hyperplasia and polycystic ovarian disease. Diurnal variation in normal men was observed. Androstenedione was measured in blood spots from neonates born at term or prematurely, with respiratory distress syndrome, or with congenital adrenal hyperplasia.
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Ballantyne, Craig S., Stuart M. Phillips, Jay R. Macdonald, Mark A. Tarnopolsky, and J. Duncan Macdougall. "The Acute Effects of Androstenedione Supplementation in Healthy Young Males." Canadian Journal of Applied Physiology 25, no. 1 (February 1, 2000): 68–78. http://dx.doi.org/10.1139/h00-005.
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We examined the effects of androstenedione supplementation on the hormonal profile of 10 males and its interaction with resistance exercise. Baseline testosterone, luteinizing hormone, estradiol, and androstenedione concentrations were established by venous sampling at 3 hr intervals over 24 hr. Subjects ingested 200 mg of androstenedione daily for 2 days, with second and third day blood samples. Two weeks later, they ingested androstenedione or a placebo for 2 days, in a double-blind, cross-over design. On day 2, they performed heavy resistance exercise with blood sampled before, after, and 90 min post. The supplement elevated plasma androstenedione 2-3-fold and luteinizing hormone ∼70% but did not alter testosterone concentration. Exercise elevated testosterone, with no difference between conditions. Exercise in the supplemented condition significantly elevated plasma estradiol by ∼83% for 90 min. Androstenedione supplementation, thus, is unlikely to provide male athletes with any anabolic benefit and, with heavy resistance exercise, elevates estrogen. Key Words: testosterone, luteinizing hormone, estradiol, fluid shifts, resistance exercise
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SHI, Haishan, Ying YANG, Weihua LI, Hui ZHANG, and Xiaolei CHENG. "Study on optimum technological conditions for producing androstenedione by microbial method." E3S Web of Conferences 136 (2019): 06025. http://dx.doi.org/10.1051/e3sconf/201913606025.
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As an indispensable intermediate, androstenedione is widely used in drug manufacturing, especially steroidal drugs. However, the chemical manufacturing process of androstenedione is generally complicated and difficult, and it will cause serious environmental pollution in the production process. The biological method for the production of androstenedione has a very promising development prospect, because it is more economical and environmentally friendly than chemical methods. In order to better produce androstenedione on a large scale, the imbalance between supply and demand can be solved. In this study, the biaqueous phase system was used to increase the substrate concentration, and the method of transforming plant sterol by mycobacterium was used to produce androstenedione. The optimal conditions for the production of androstenedione by microbial assay were determined by orthogonal test: the aqueous two-phase system was water/ sunflower oil, the temperature was 30 °C, the initial pH was 6.5, the substrate concentration was 0.4 g/L, the rotation speed was 250 rpm, and the inoculation was carried out. The amount was 14.83%, the organic ratio was 20.65%, and the liquid loading was 150/500 mL. The preliminary production of androstenedione by microbial method has found suitable process conditions and provided data and theoretical support for its large-scale production.
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Janeczko, Anna, Maciej Kocurek, and Izabela Marcińska. "Mammalian androgen stimulates photosynthesis in drought-stressed soybean." Open Life Sciences 7, no. 5 (October 1, 2012): 902–9. http://dx.doi.org/10.2478/s11535-012-0068-6.
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AbstractThe aim of the present studies was to assess the possibility of compensating the negative effects of drought stress on gaseous exchange and efficiency of photosystem II in soybean seedlings by application of the androgen — androstenedione. Androstenedione (0.25 mg dm−3) was applied via presowing seed soaking (12 h). Control seeds were untreated with steroid. Plants were cultured in pots. On the 12th day of growth, the plants were watered for the last time. Drought symptoms occurred during the next 10 days. On the 22nd day of growth, leaf gaseous exchange and PSII measurements were taken. Afterwards the plants were watered. Two days later measurements were taken again. Androstenedione improved the intensity of leaf net photosynthesis. The effect of androstenedione was manifested during the rehydration of plants that have undergone a period of drought. An increase in net photosynthesis intensity was accompanied by higher transpiration. Possible mechanisms of androstenedione action — effect on aquaporin functionality and membrane stability — are discussed. The significance of ethanol and DMSO (solvents of steroid) in experiments on the physiological activity of androstenedione is also considered.
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Byrne, Bridgette, Sean Cunningham, Derval Igoe, Ronan Conroy, and T. Joseph McKenna. "Sex steroids, adiposity and smoking in the pathogenesis of idiopathic hirsutism and polycystic ovary syndrome." Acta Endocrinologica 124, no. 4 (April 1991): 370–74. http://dx.doi.org/10.1530/acta.0.1240370.
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Abstract. Hyperestronemia may be central to the development of polycystic ovary syndrome. The present study was designed to examine whether increased availability of androstenedione or increased aromatase closely associated with adiposity, plays the dominant role in the development of hyperestronemia. We measured plasma androstenedione, estrone and the estrone/androstenedione ratio (an indirect index of peripheral aromatase activity), in 141 patients with idiopathic hirsutism and in 88 patients with polycystic ovary syndrome. Estrone levels were higher in polycystic ovary syndrome, 250.4±129 (mean ± standard deviation) than in idiopathic hirsutism, 210.6±119 pmol/l, p<0.05. Plasma androstenedione levels were higher in polycystic ovary syndrome, 8.24±3.5, than in idiopathic hirsutism, 7.1±1.7 nmol/l, p<0.0025. However, the estrone/androstenedione ratio was similar in the two groups. In all patients who smoked, androstenedione was higher, 8.14±3.22 than in non-smokers, 6.99±2.96 nmol/l, p<0.005. Smokers had a lower body mass index, 23.9±2.3, than non-smokers 25.6±4.8 kg/m2, p<0.025. However, estrone levels were similar in smokers and in non-smokers. These data indicate that elevated estrone is more closely related to increased availability of androstenedione than to increased aromatase activity. While cigarette smoking appears to increase androstenedione levels, it may inhibit aromatase activity either directly or indirectly because of an associated reduction in adiposity. However, since the relative frequency of polycystic ovary syndrome and idiopathic hirsutism was similar in smokers and non-smokers, smoking did not appear to reduce estrone bioactivity as had been claimed.
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Pouliot, Frederic, Mélanie Rouleau, Bertrand Neveu, Paul Toren, Fannie Morin, Lauriane Vélot, Keyue Ding, et al. "Contribution of extragonadal steroids to the androgen receptor activity and to the castration-resistance development in recurrent prostate cancers after primary therapy." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 148. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.148.
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148 Background: Beyond testosterone, several steroids contribute to the activation of the androgen receptor (AR) pathway, but their relative contributions in castrated prostate cancer (PCa) patients remain unknown. Methods: Serum levels of nine steroids were measured by mass spectrometry from continuously castrated patients of the PR.7 study (n=219) and from the PCA24 cohort (n=116). For each steroid, standard curves for dose-dependent prostate-specific antigen promoter activation were built in castration-sensitive (LAPC4) and resistant (VCaP) PCa models. Standard curves were used to determine the AR activation potency for each steroid measurement from patients. Results: In LAPC4 and VCaP cells, testosterone, dihydrotestosterone and androstenedione induced AR transcriptional activity, while dehydroepiandrosterone, 5alpha-androstan-3beta,17beta-diol, androstenediol, androsterone stimulated AR only in VCaP cells. Extragonadal steroids were responsible for 34% (LAPC4) and 88% (VCaP) of the serum total AR transcriptional activity found in castrated patients. The total AR transcriptional activity secondary to testosterone, dihydrotestosterone and androstenedione was associated with time to castration resistance in patients from the PR.7 study (HR=2.17; 95% CI: 1.12-4.23; p=0.02) in multivariate analysis using the castration-sensitive model (LAPC4). AR transcriptional activity of extragonadal androstenedione was the only steroid statistically associated with time to castration resistance in univariate analysis (HR=1.89; 95% CI: 1.04-3.44; p=0.036). Conclusions: Extragonadal steroids contribute significantly to the AR axis activation at testosterone castration levels in recurrent non-metastatic PCa and these sustain the development of castration resistance after primary local treatment.
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Krishna, A., and P. F. Terranova. "Relationships between LH stimulation in vitro and progesterone, androstenedione and cyclic AMP synthesis in preantral follicles of the cyclic hamster." Journal of Endocrinology 114, no. 1 (July 1987): 55–63. http://dx.doi.org/10.1677/joe.0.1140055.
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ABSTRACT In-vivo changes in steroidogenesis in preantral hamster follicles following exposure to the LH surge could be mimicked by stimulation with exogenous LH in vitro. Luteinizing hormone given only during the first hour (media were changed every hour) of a 6-h incubation promptly increased the concentration of androstenedione and adenosine 3′:5′-monophosphate (cAMP) in the media and this was followed by a gradual decline to <20% of the peak value; progesterone in media was not detectable with a single LH stimulation. However, LH given every hour increased progesterone and cAMP concentrations in the media throughout the period of incubation, but the transient increase and subsequent decline in androstenedione was still observed. The decline in androstenedione release by preantral follicles was apparently due to a lack of steroid precursor and not to either inhibition of hydroxyl-lyase or lack of LH or cAMP stimulation. Exogenous dibutyryl cAMP (dbcAMP) and 8-Br-cAMP mimicked the effects of LH on the pattern of follicular androstenedione release into the media; however, dbcAMP and 8-Br-cAMP did not increase concentrations of progesterone in vitro. In preantral follicles, LH stimulated cAMP release into the media and apparently inhibited phosphodiesterase activity, since methyl isobutylxanthine (MIX) did not potentiate the effect of LH on cAMP. Follicle-stimulating hormone also increased androstenedione and cAMP in the media of the preantral follicles in a manner similar to that of LH, except that between 4 and 6 h of incubation the release of androstenedione and cAMP was less than that produced by stimulation with LH. Interestingly, FSH and MIX stimulated androstenedione and cAMP release by preantral follicles in a manner similar to that induced by LH alone. These results indicate that LH stimulation of preantral follicles in vitro induces an androstenedione– progesterone shift which is mediated by cAMP. The decline in androstenedione release by the preantral follicle in vitro appears to be due to a lack of appropriate steroid precursors and not to an inhibitory action of LH on androgen synthesis. J. Endocr. (1987) 114, 55–63
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Schnirring, Lisa. "Androstenedione et al: Nonprescription Steroids." Physician and Sportsmedicine 26, no. 11 (November 1998): 15–18. http://dx.doi.org/10.3810/psm.1998.11.1509.
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De Cree, Carl. "Androstenedione and dehydroepiandrosterone for athletes." Lancet 354, no. 9180 (August 1999): 779–80. http://dx.doi.org/10.1016/s0140-6736(05)76025-6.
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Craig, B. W., D. Biggs, C. Fick, D. Wright, and K. Lim. "ANDROSTENEDIONE SUPPLEMENTATION IN ELDERLY MEN." Medicine & Science in Sports & Exercise 34, no. 5 (May 2002): S231. http://dx.doi.org/10.1097/00005768-200205001-01297.
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&NA;. "Androstenedione alters sex hormone levels." Inpharma Weekly &NA;, no. 1225 (February 2000): 19. http://dx.doi.org/10.2165/00128413-200012250-00051.
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Beckham, S. G., and C. P. Earnest. "ANDROSTENEDIONE SUPPLEMENTATION IN OLDER MEN." Medicine & Science in Sports & Exercise 33, no. 5 (May 2001): S339. http://dx.doi.org/10.1097/00005768-200105001-01908.
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Brown, Gregory A., Matthew D. Vukovich, Emily R. Martini, Marian L. Kohut, Warren D. Franke, David A. Jackson, and Douglas S. King. "Effects of Androstenedione-Herbal Supplementation on Serum Sex Hormone Concentrations in 30- to 59-Year-old Men." International Journal for Vitamin and Nutrition Research 71, no. 5 (September 1, 2001): 293–301. http://dx.doi.org/10.1024/0300-9831.71.5.293.
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The effectiveness of a nutritional supplement designed to enhance serum testosterone concentrations and prevent the formation of dihydrotestosterone and estrogens from the ingested androgens was investigated in healthy 30- to 59-year old men. Subjects were randomly assigned to consume DION (300 mg androstenedione, 150 mg dehydroepiandrosterone, 540 mg saw palmetto, 300 mg indole-3-carbinol, 625 mg chrysin, and 750 mg Tribulus terrestris per day; n = 28) or placebo (n = 27) for 28 days. Serum free testosterone, total testosterone, androstenedione, dihydrotestosterone, estradiol, prostate-specific antigen (PSA), and lipid concentrations were measured before and throughout the 4-week supplementation period. Serum concentrations of total testosterone and PSA were unchanged by supplementation. DION increased (p < 0.05) serum androstenedione (342%), free testosterone (38%), dihydrotestosterone (71%), and estradiol (103%) concentrations. Serum HDL-C concentrations were reduced by 5.0 mg/dL in DION (p < 0.05). Increases in serum free testosterone (r2 = 0.01), androstenedione (r2 = 0.01), dihydrotestosterone (r2 = 0.03), or estradiol (r2 = 0.07) concentrations in DION were not related to age. While the ingestion of androstenedione combined with herbal products increased serum free testosterone concentrations in older men, these herbal products did not prevent the conversion of ingested androstenedione to estradiol and dihydrotestosterone.
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Hojo, Yasushi, Shimpei Higo, Hirotaka Ishii, Yuuki Ooishi, Hideo Mukai, Gen Murakami, Toshihiro Kominami, et al. "Comparison between Hippocampus-Synthesized and Circulation-Derived Sex Steroids in the Hippocampus." Endocrinology 150, no. 11 (July 9, 2009): 5106–12. http://dx.doi.org/10.1210/en.2009-0305.
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Estradiol (E2) and other sex steroids play essential roles in the modulation of synaptic plasticity and neuroprotection in the hippocampus. To clarify the mechanisms for these events, it is important to determine the respective role of circulating vs. locally produced sex steroids in the male hippocampus. Liquid chromatography-tandem mass spectrometry in combination with novel derivatization was employed to determine the concentration of sex steroids in adult male rat hippocampus. The hippocampal levels of 17β-E2, testosterone (T), and dihydrotestosterone (DHT) were 8.4, 16.9, and 6.6 nm, respectively, and these levels were significantly higher than circulating levels. The hippocampal estrone (E1) level was, in contrast, very low around 0.015 nm. After castration to deplete circulating high level T, hippocampal levels of T and DHT decreased considerably to 18 and 3%, respectively, whereas E2 level only slightly decreased to 83%. The strong reduction in hippocampal DHT resulting from castration implies that circulating T may be a main origin of DHT. In combination with results obtained from metabolism analysis of [3H]steroids, we suggest that male hippocampal E2 synthesis pathway may be androstenedione → T → E2 or dehydroepiandrosterone → androstenediol → T → E2 but not androstenedione → E1 → E2.
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Bubenik, G. A., D. K. Pomerantz, D. Schams, and P. S. Smith. "The role of androstenedione and testosterone in the reproduction and antler growth of a male white-tailed deer." Acta Endocrinologica 114, no. 1 (January 1987): 147–52. http://dx.doi.org/10.1530/acta.0.1140147.
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Abstract. Seasonal levels of androstenedione and testosterone were investigated in plasma of mature intact and castrated male white-tailed deer. In four intact bucks, androstenedione concentrations were low in February and March (around 1 nmol/l) and then increased significantly (P < 0.05) from April to November (peak 2.34 nmol/l). Testosterone remained low (below 3.5 nmol/l) from February to August and then rose significantly (P < 0.01) till November (peak 36.78 nmol/l). Both hormones declined from November to February. In three castrates, androstenedione levels remained virtually unchanged (averaging around 0.5 nmol/l) between January and September. After a rapid significant increase (P < 0.05) till November (peak value 2.45 nmol/l), androstenedione concentrations declined quickly to a baseline level. Testosterone in castrates remained around 0.3 to 0.7 nmol/l for most of the year with a non-significant peak (1.45 nmol/l) in October. These data indicate that the spring and summer increase in androstenedione in the intact deer is of testicular origin; the fall peak, however, may be a result of increased production in the adrenal glands. It can be speculated that the increase in androstenedione in the blood of the male deer during the spring may be responsible for the seasonal initiation and support of antler growth as well as being supportive to the re-activation of the reproductive system.
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Kushnir, Mark M., Takara Blamires, Alan L. Rockwood, William L. Roberts, Bingfang Yue, Evrim Erdogan, Ashley M. Bunker, and A. Wayne Meikle. "Liquid Chromatography–Tandem Mass Spectrometry Assay for Androstenedione, Dehydroepiandrosterone, and Testosterone with Pediatric and Adult Reference Intervals." Clinical Chemistry 56, no. 7 (July 1, 2010): 1138–47. http://dx.doi.org/10.1373/clinchem.2010.143222.
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Abstract Background: Measurement of serum androgens is important in adult, geriatric, pediatric endocrinology, and oncology patients. We developed a liquid chromatography—tandem mass spectrometry (LC-MS/MS) assay for simultaneous measurement of androstenedione, dehydroepiandrosterone (DHEA), and testosterone in these patients. Methods: We spiked 200 μL of serum or plasma with isotope-labeled internal standards and performed extraction with methyl t-butyl ether. We then derivatized the extracts with hydroxylamine and analyzed them by LC-MS/MS using a 2-dimensional chromatographic separation with a 3.5-min analysis time. Results: Total imprecision for each analyte was <11.2%. Limits of quantification were 10, 50, and 10 ng/L for androstenedione, DHEA, and testosterone, respectively. Reference intervals were established for children (age 6 months to 17 years), men, and women. Androstenedione and DHEA concentrations were lowest in 2- to 3-year-old children. Adult concentrations were achieved in girls at Tanner stage 3 and in boys at Tanner stage 4–5. In premenopausal and (postmenopausal) women the median concentrations of androstenedione, DHEA, and testosterone were 810 (360), 3000 (1670), 270 (180) ng/L, respectively. In postmenopausal women, concentrations of testosterone were age independent, whereas androstenedione and DHEA concentrations decreased with age. In men the median concentrations of androstenedione, DHEA, and testosterone were 440, 2000, and 3700 ng/L, respectively. In men older than 40 years, median concentrations decreased at rates of 5%, 10%, and 20% per decade for androstenedione, DHEA, and testosterone, respectively. Conclusions: This LC-MS/MS method has the required lower limit of quantification and specificity for analysis of endogenous concentrations of androgens in all groups studied. Reference intervals were established for healthy children and adults.
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Ferraris, Jorge R., José A. Ramírez, Victoria Goldberg, and Marco A. Rivarola. "Glucocorticoids and adrenal androgens in children with end stage renal disease." Acta Endocrinologica 124, no. 3 (March 1991): 245–50. http://dx.doi.org/10.1530/acta.0.1240245.
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Abstract. We studied the effects of chronic renal failure on the pituitary-cortisol axis and adrenal androgen function in 26 patients (16 male and 10 female), aged 6.5 to 22.5 years (mean 14.5). Ten patients were prepubertal, 8 pubertal, and 8 post-pubertal. All of them were on chronic hemodialysis. Pubic hair development was delayed in 56% of the patients. Serum cortisol was increased in 15 out of the 26 patients. Serum Δ4-androstenedione was high in 11 out of 15 patients in Tanner's stage I or II and in 1 out of 11 patients in Tanner's stage III, IV or V (p<0.01). Serum cortisol was elevated in 10 out of 12 patients with high serum Δ4-androstenedione and in only 5 out of 14 with normal Δ4-androstenedione (p<0.02). Serum dehydroepiandrosterone sulphate was normal in 22 patients and elevated in 4 males. There was a significant inverse correlation between bone age and serum cortisol (r:-0.59; p<0.005) and a significant positive correlation between bone age and serum dehydroepiandrosterone sulphate (r: 0.45 p<0.01). Serum ACTH was normal. A reduction by 50% in cortisol and 78% in dehydroepiandrosterone sulphate was found after dexamethasone suppression, but Δ4-androstenedione did not suppress after dexamethasone. After ACTH stimulation test cortisol increased by 50% and Δ4-androstenedione by 80%. Conclusions: The increased levels of cortisol and Δ4-androstenedione with partial resistance to dexamethasone suggest that these patients have a hypothalamic-pituitary dysfunction similar to that found in Cushing's disease or in chronic stress. The difference in the responses of Δ4-androstenedione and dehydroepiandrosterone sulphate observed is consistent with the existence of different mechanisms of control for these two steroids.
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Patil, Prachi, Rajesh Sharma, Tushar Banerjee, and Shridhar Patil. "SUBSTRATE CARRIERS FOR C-1(2)-DEHYDROGENATION OF 6-METHYLENE ANDROSTENEDIONE TO EXEMESTANE BY GROWING AND IMMOBILIZED ARTHROBACTER SIMPLEX NCIM 2449." Asian Journal of Pharmaceutical and Clinical Research 10, no. 2 (February 1, 2017): 392. http://dx.doi.org/10.22159/ajpcr.2017.v10i2.15861.
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Objective: Permeability of hydrophobic steroid substrates across cell membrane is a critical factor during microbial bioconversion. To increase substrate intake, the feasibility of some organic solvents and emulsifiers as substrate carrier on the bioconversion of 6-methylene androstenedione to exemestane was assessed.Methods: Androstenedione, a commonly available steroid precursor, was chemically converted 6-methylene androstenedione. The time course of exemestane accumulation was estimated after addition of 6-methylene androstenedione dissolved in some organic solvents or dispersed with emulsifiers by growing and immobilized cells of Arthrobacter simplex NCIM 2449 in shake flask cultures. Results: The use of substrate carriers for addition of 6-methylene androstenedione enhanced the bioconversion several folds. With growing bacterium in triplicate flasks, a peak mol % bioconversion recorded was- ethanol (67.25, 72 h); soybean oil + tween 80 (50.37, 48 h); acetone (38.84, 48 h); soybean oil (38.36, 48 h); lecithin (32.73, 48 h), methanol (32.71, 48 h) and tween 80 (10.37, 48 h). As compared to the growing cells, the bioconversion with Ca-alginate immobilized cells was delayed and peak mol % bioconversion was recorded as ethanol (60.78, 120 h); soybean oil + tween 80 (42.98, 120 h); methanol (40.50, 72 h); soybean oil (38.36, 48 h); acetone (31.18, 72h ) and lecithin (33.67, 120 h); tween 80 (13.87, 120 h).Conclusion: The use of substrate carriers for addition of 6-methylene androstenedione increased the permeability of substrate and may be used to increase the yield of exemestane and reduce incubation time.
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Taketsuru, Hiroaki, Yuji Hirao, Naoki Takenouchi, Kosuke Iga, and Takashi Miyano. "Effect of androstenedione on the growth and meiotic competence of bovine oocytes from early antral follicles." Zygote 20, no. 4 (November 9, 2011): 407–15. http://dx.doi.org/10.1017/s0967199411000268.
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SummaryMedium that contains 17β-estradiol has been reported to support in vitro growth of bovine oocytes, isolated from early antral follicles, until the final stage. The aim of this study was to determine the effects of androstenedione in medium on such growing bovine oocytes. Oocyte–granulosa cell complexes were collected from early antral follicles and cultured for 14 days in medium supplemented with 17β-estradiol (0, 10 and 100 ng/ml) or androstenedione (0, 10 and 100 ng/ml). The mean diameter of oocytes measured after seeding on the culture substrate was 96.9 μm (n = 191). Either steroid was necessary for maintainance of the organization of oocyte–granulosa cell complexes over the 14-day culture period. In the 17β-estradiol- or the androstenedione-supplemented medium about 80% or 65%, respectively, of viable oocytes were recovered. In both groups the increase in oocyte size was significant after 14 days. The in vitro grown oocytes were cultured for a further 22–24 h for oocyte maturation; 13% and 30% of oocytes grown in the 10 and 100 ng/ml 17β-estradiol-supplemented medium reached metaphase II, respectively; more than 64% of oocytes grown in the androstenedione-supplemented medium matured to metaphase II. These results show that androstenedione, as 17β-estradiol, can maintain the viability of bovine oocyte–granulosa cell complexes and support the growth of oocytes, and that androstenedione promotes the acquisition of oocyte meiotic competence efficiently at a low dose.
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Bradshaw, K. D., L. Milewich, J. I. Mason, C. R. Parker, P. C. MacDonald, and B. R. Carr. "Steroid secretory characteristics of a virilizing adrenal adenoma in a woman." Journal of Endocrinology 140, no. 2 (February 1994): 297–307. http://dx.doi.org/10.1677/joe.0.1400297.
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Abstract A tumour of the left adrenal gland was identified in a woman who presented with virilization and secondary amenorrhea. Preoperatively, the plasma levels of dehydroepiandrosterone sulphate, dehydroepiandrosterone, androstenedione, testosterone, 5α-dihydrotestosterone and 5-androstene-3β,17β-diol were elevated two- to fourfold whereas those of urinary 17-ketosteroids were elevated more than tenfold. The production rate of dehydroepiandrosterone sulphate was more than 16 times that in normal women whereas those of dehydroepiandrosterone, testosterone and androstenedione were approximately twofold greater; plasma testosterone was derived almost entirely from the peripheral conversion of androstenedione. Blood was obtained by catheterization of the ovarian veins, left adrenal gland vein and inferior vena cava (at two different sites) and plasma steroid levels were determined: testosterone and cortisol levels were elevated in all blood samples whereas those of androstenedione, dehydroepiandrosterone sulphate and 11-desoxycortisol were approximately six- to eightfold, 1·5-fold and nine- to 22-fold higher in the effluent of the left adrenal gland/tumour compared with the levels in the other compartments. Blood was collected hourly for 24 h to determine steroid levels under basal conditions and, also, after ACTH treatment. Plasma cortisol levels increased markedly upon ACTH administration and fell to very low levels 11 h later, but those of androstenedione, testosterone, dehydroepiandrosterone, 5-androstene-3β,17β-diol and dehydroepiandrosterone sulphate were not affected by ACTH treatment. A histological diagnosis of cortical adenoma of the extirpated tumour was made. Tissue explants and adenoma cells were maintained in culture to characterize the steroid-metabolizing properties of the tumour. The secretion of dehydroepiandrosterone sulphate by tissue explants was high initially, but declined to almost undetectable levels after 5 days in culture. In the presence of ACTH, dehydroepiandrosterone sulphate secretion remained elevated throughout the entire study up to 5 days. Basal secretion of dehydroepiandrosterone sulphate, androstenedione, 11-desoxycortisol, cortisol, testosterone and 11β-hydroxyandrostenedione by adenoma cells was either very low or undetectable. In the presence of ACTH, dibutyryl cyclic AMP or cholera toxin the secretion of dehydroepiandrosterone sulphate, androstenedione and 11-desoxycortisol increased markedly with time in culture up to 3 days, whereas the other steroids were undetected in the medium. A homogenate of adenoma tissue metabolized testosterone to androstenedione, but the conversion of androstenedione to testosterone was minimal. The findings of this study served to establish that virilization in this woman was due, at least in part, to excess testosterone – and testosterone-derived 5α-dihydrotestosterone – produced at extra-adrenal tissue sites almost exclusively through metabolism of tumour-secreted androstenedione. The excess production of steroid prohormones in this woman was due to autonomous tumour steroidogenesis. The remarkable feature was the degree of virilization resulting from a modest increase in biologically potent androgens. Journal of Endocrinology (1994) 140, 297–307
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Kamińska, Barbara, M. Opalka, and Luiza Dusza. "Phytoestrogens alter cortisol and and rostenedione secretion by porcine adrenocortical cells." Acta Veterinaria Hungarica 55, no. 3 (September 1, 2007): 359–67. http://dx.doi.org/10.1556/avet.55.2007.3.10.
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The effect of plant-derived, nonsteroidal estrogens (genistein, daidzein and biochanin A) on cortisol and androstenedione secretion by porcine adrenocortical cells was examined. Adrenals were harvested from locally slaughtered mature gilts on days 5–9 of the oestrous cycle. Adrenocortical cells were incubated with or without genistein, daidzein, biochanin A (0.5, 5, 10 or 50 μM), oestradiol (10, 50, 100 or 500 pg/mL) and ACTH (5 nM — positive control). All incubations were performed for 8 h (95% air and 5% CO 2 , 37°C). ACTH increased cortisol and androstenedione secretion. Genistein, daidzein and biochanin A suppressed cortisol output, whereas androstenedione secretion was enhanced by these phytoestrogens. In contrast, oestradiol did not alter steroid secretion by porcine adrenocortical cells, which may suggest that phytoestrogens have a non-oestrogenic mechanism of action. Therefore, phytoestrogens present in commercial forage may influence adrenocortical function in pigs by decreasing cortisol and increasing androstenedione secretion.
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Carlberg, K. A., B. L. Alvin, and A. R. Gwosdow. "Exercise during pregnancy and maternal and fetal plasma corticosterone and androstenedione in rats." American Journal of Physiology-Endocrinology and Metabolism 271, no. 5 (November 1, 1996): E896—E902. http://dx.doi.org/10.1152/ajpendo.1996.271.5.e896.
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Adrenocortical glucocorticoid and androgen secretion is stimulated by exercise. Excesses of these hormones in fetuses can cause abnormalities in development. We measured maternal and fetal plasma corticosterone and androstenedione concentrations in Sprague-Dawley rats immediately after maternal exercise in exercise-trained mothers and at rest in sedentary mothers. To do this, we developed a technique for fetal blood sampling and assessed its effect on maternal and fetal plasma corticosterone concentrations. Under halothane anesthesia, maternal blood was collected by cardiac puncture and fetal blood was collected from carotid and jugular vessels. Corticosterone was not affected by the blood collection procedure. Corticosterone was significantly higher in exercised mothers and their fetuses after 30 min of running than in sedentary mothers and their fetuses at rest. Androstenedione was significantly higher in exercised mothers after 30 min of running than in sedentary mothers at rest, but fetal androstenedione was not different between groups. We conclude that this maternal exercise protocol elevates plasma corticosterone but not androstenedione concentrations in fetal rats.
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Burduli, Anna G., Natalia A. Kitsilovskaya, Yuliya V. Sukhova, Irina A. Vedikhina, Tatiana Yu Ivanets, Vitaliy V. Chagovets, Nataliia L. Starodubtseva, and Vladimir E. Frankevich. "Androstenedione as a potential predictor of ovarian response in assisted reproductive technology programs." Gynecology 22, no. 1 (May 1, 2020): 38–44. http://dx.doi.org/10.26442/20795696.2020.1.200010.
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Aim. To assess the possibility of using androstenedione levels in blood serum and follicular fluid to predict ovarian response in assisted reproductive technology programs and to conduct a comparative analysis of the results obtained by 2 methods chemiluminescent immunoassay (CLIA) and high-performance liquid chromatography-mass spectrometry (HPLC-MS/MS).
Materials and methods. A prospective study included 55 couples who received in vitro fertilization/intracytoplasmic sperm injection and embryo transfer program therapy. The patients were divided into 3 groups depending on the ovarian response to stimulation: 1st (13 oocytes, n=4), 2nd (49 oocytes, n=27), 3rd (over 10 oocytes, n=24). Androstenedione levels were measured in blood serum obtained on the day of transvaginal ovarian puncture and in follicular fluid samples with CLIA and HPLC-MS/ MS methods at the laboratories of Kulakov National Medical Research Center of Obstetrics, Gynecology and Perinatology.
Results. On the day of transvaginal ovarian puncture, the serum androstenedione levels, which were measured by HPLC-MS/MS, were increasing with an increase of the number of oocytes obtained. The CLIA method revealed a difference in the androstenedione levels between the groups with the number of oocytes obtained of less than 3 and more than 10. Moreover, the androstenedione levels measured by CLIA were significantly different between the patient groups (p0.05).
Comparison of serum androstenedione levels measured by CLIA and HPLC-MS/MS, showed high correlations between the values [=0.73 (p0.001)], which makes it possible to use both methods equally, given the existing equipment of the clinical base.
Conclusion. Prediction of ovarian response to stimulation is an important step in assisted reproductive technology programs. Measuring androstenedione concentration in blood serum on the day of transvaginal ovarian puncture with highly specific methods (CLIA and HPLC-MS/MS) can be used to predict the degree of ovarian response along with the traditional assessment of the ovarian reserve based on determining anti-Mullerian hormone levels in the early follicular phase of the menstrual cycle.
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Ehrhart-Bornstein, Monika, Stefan R. Bornstein, Heike Güse-Behling, Hans G. Stromeyer, Torben N. Rasmussen, Werner A. Scherbaum, Guido Adler, and Jens J. Holst. "Sympathoadrenal Regulation of Adrenal Androstenedione Release." Neuroendocrinology 59, no. 4 (1994): 406–12. http://dx.doi.org/10.1159/000126685.
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Johnston, S., C. Cribbs, H. Aukema, and N. DiMarco. "ANDROSTENEDIONE SUPPLEMENTATION AND POLYCYSTIC KIDNEY DISEASE." Medicine & Science in Sports & Exercise 33, no. 5 (May 2001): S339. http://dx.doi.org/10.1097/00005768-200105001-01909.
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Preti, M. S., O. Magrini, S. Lodi, C. Melega, R. Paradisi, and C. Flamigni. "Direct Enzyme-Immunoassay for Plasma Androstenedione." Analytical Letters 24, no. 7 (July 1991): 1125–36. http://dx.doi.org/10.1080/00032719108052958.
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Eggleston, D. S., and H. Y. Lan-Hargest. "6α- and 6β-Trifluoromethyl-substituted androstenedione." Acta Crystallographica Section C Crystal Structure Communications 46, no. 9 (September 15, 1990): 1686–91. http://dx.doi.org/10.1107/s0108270189012400.
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Purnell, B. A. "EVOLUTION: An Early Use of Androstenedione." Science 317, no. 5839 (August 10, 2007): 723d. http://dx.doi.org/10.1126/science.317.5839.723d.
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Tang, Weiwei, Chuang Xie, Zhao Wang, Songgu Wu, Ying Feng, Xuemei Wang, Jingkang Wang, and Junbo Gong. "Solubility of androstenedione in lower alcohols." Fluid Phase Equilibria 363 (February 2014): 86–96. http://dx.doi.org/10.1016/j.fluid.2013.11.008.
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Malaviya, Alok, and James Gomes. "Androstenedione production by biotransformation of phytosterols." Bioresource Technology 99, no. 15 (October 2008): 6725–37. http://dx.doi.org/10.1016/j.biortech.2008.01.039.
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Sahu, Saura C., Philip P. Sapienza, Robert L. Sprando, Thomas F. X. Collins, Ivan A. Ross, Thomas J. Flynn, Paddy L. Wiesenfeld, Michael W. O’Donnell, and Chung S. Kim. "Hepatotoxicity of androstenedione in pregnant rats." Food and Chemical Toxicology 43, no. 2 (February 2005): 341–44. http://dx.doi.org/10.1016/j.fct.2004.11.005.
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Milewich, Leon, Valsala Kaimal, Cynthia B. Shaw, and Alice R. Johnson. "Androstenedione metabolism in human lung fibroblasts." Journal of Steroid Biochemistry 24, no. 4 (April 1986): 893–97. http://dx.doi.org/10.1016/0022-4731(86)90451-6.
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Young, J. M., and A. S. McNeilly. "Inhibin removes the inhibitory effects of activin on steroid enzyme expression and androgen production by normal ovarian thecal cells." Journal of Molecular Endocrinology 48, no. 1 (November 14, 2011): 49–60. http://dx.doi.org/10.1530/jme-11-0134.
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Activin and inhibin are important local modulators of theca cell steroidogenesis in the ovary. Using a serum-free primary theca cell culture system, this study investigated the effects of inhibin on theca cell androgen production and expression of steroidogenic enzymes. Androstenedione secretion from theca cells cultured in media containing activin, inhibin and follistatin was assessed by RIA over 144 h. Activin (1–100 ng/ml) suppressed androstenedione production. Inhibin (1–100 ng/ml) blocked the suppressive effects of added activin, but increased androstenedione production when added alone, suggesting it was blocking endogenous activin produced by theca cells. Addition of SB-431542 (activin receptor inhibitor) and follistatin (500 ng/ml) increased androstenedione production, supporting this concept. Infection of theca cells with adenoviruses expressing inhibitory Smad6 or 7 increased androstenedione secretion, confirming that the suppressive effects of activin required activation of the Smad2/3 pathway. Activin decreased the expression levels of steroidogenic acute regulatory protein (STAR), whereas STAR expression was increased by inhibin and SB-431542, alone and in combination. CYP11A was unaffected. The expression of CYP17 encoding 17α-hydroxylase was unaffected by activin but increased by inhibin and SB-431542, and when added in combination the effect was further enhanced. The expression of 3β-hydroxysteroid dehydrogenase (3β-HSD) was significantly decreased by activin, while inhibin alone and in combination with SB-431542 both potently increased the expression of 3β-HSD. In conclusion, activin suppressed theca cell androstenedione production by decreasing the expression of STAR and 3β-HSD. Inhibin and other blockers of activin action reversed this effect, supporting the concept that endogenous thecal activin modulates androgen production in theca cells.
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Phillips, Gerald B. "Relationship between serum dehydroepiandrosterone sulfate, androstenedione, and sex hormones in men and women." European Journal of Endocrinology 134, no. 2 (February 1996): 201–6. http://dx.doi.org/10.1530/eje.0.1340201.
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Phillips GB. Relationship between serum dehydroepiandrosterone sulfate, androstenedione, and sex hormones in men and women. Eur J Endocrinol 1996;134:201–6. ISSN 0804–4643 Previous reports of a correlation between serum dehydroepiandrosterone sulfate (DHEAS) and testosterone in both men and women have led to the suggestion that adrenal and gonadal secretion are related. In the present study, the correlation of DHEAS with testosterone and free testosterone (FT) in both normal men and women was tested. Androstenedione, estradiol, sex hormone binding globulin (SHBG), and insulin were also measured and their correlations determined. All correlations were controlled for age and body mass index. In the men in the study, DHEAS did not correlate with testosterone or FT but correlated strongly with androstenedione. In the women, DHEAS correlated strongly with testosterone, FT. and androstenedione; androstenedione in turn correlated strongly with testosterone and FT. DHEAS showed no correlations with estradiol, SHBG, or insulin in the men or women. The lack of a correlation between DHEAS and testosterone in normal men is consistent with the independent secretion of these hormones by the adrenal and testis, respectively. The finding of a strong DHEAS-testosterone correlation in normal women may be explained by parallel adrenal secretion in response to trophic stimuli, i.e., without invoking an adrenal-gonadal interaction. GB Phillips, Roosevelt Hospital, 428 West 59th Street, New York, NY 10019, USA
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Tsang, Benjamin K., Arezoo Taheri, Louis Ainsworth, and Bruce R. Downey. "Secretion of 17α-hydroxyprogesterone, androstenedione, and estrogens by porcine granulosa and theca interna cells in culture." Canadian Journal of Physiology and Pharmacology 65, no. 9 (September 1, 1987): 1951–56. http://dx.doi.org/10.1139/y87-304.
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The steroid secreting activities of dispersed granulosa and theca interna cells from preovulatory follicles of prepubertal gilts 72 h after pregnant mare's serum gonadotropin treatment (750 IU) were compared. The cells were cultured for 24 h with or without steroid substrate (10−8 to 10−5 M progesterone, 17α-hydroxyprogesterone, or androstenedione), FSH (100 ng/mL), LH (100 ng/mL), and cyanoketone (0.25 μM, an inhibitor of 3β-hydroxysteroid dehydrogenase). Granulosa cells cultured alone secreted mainly progesterone. Theca interna cells secreted mainly 17α-hydroxyprogesterone and androstenedione, with secretion being markedly enhanced by LH. In the presence of cyanoketone, which inhibited endogenous progesterone production, theca interna but not granulosa cells were able to convert exogenous progesterone to 17α-hydroxyprogesterone and androstenedione, and exogenous 17α-hydroxyprogesterone to androstenedione and estradiol-17β in high yield. The secretion of the latter steroids from exogenous substrates was unaffected by LH. Theca interna cells secreted more estradiol-17β than did granulosa cells in the absence of aromatizable substrate, but estradiol-17β secretion by the latter was markedly increased after the addition of androstenedione. These apparent differences in steroid secreting activity between the cell types suggest that the enzymes responsible for conversion of C21 to C19 steroids, i.e., 17α-hydroxylase and C17,20-lyase, reside principally in the theca interna cells. However, aromatase activity appears to be much higher in granulosa cells.
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Tomei, G., A. Sancini, D. Cerratti, M. Fiaschetti, M. F. Anzani, M. Ciarrocca, M. V. Rosati, et al. "Effects on Plasmatic Androstenedione in Female Workers Exposed to Urban Stressors." European Journal of Inflammation 7, no. 3 (September 2009): 175–81. http://dx.doi.org/10.1177/1721727x0900700308.
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The purpose of this study is to investigate whether occupational exposure to urban stressors can cause alterations on androstenedione plasma levels and related diseases in female traffic police compared to a control group. The research was carried out on an initial sample of 468 female workers (209 traffic police and 259 controls). After excluding the subjects with confounding factors, 192 female subjects: 96 traffic police and 96 controls were included in the study. Traffic police and controls were matched by age, length of service, body mass index, alcohol consumption and cigarette smoking habits, habitual consumption of Italian coffee, and habitual intake of soy and liquorice in diet. The results show that the percentage of subjects with fertility and mental health disorders were no different between traffic police and controls. Mean androstenedione values were significantly higher in female traffic police compared to controls. The distribution into classes of androstenedione values in traffic police was statistically significant. The percentage of traffic police with fertility and mental health disorders were not significant compared to controls. Our results suggest that the occupational exposure to urban stressors could alter plasma androstenedione levels in female traffic police. According to our previous research all the hormonal parameters studied, including androstenedione, could be used as early biological markers of chronic exposure to urban stressors, usable in occupational sets.
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Wei, Ruhan, Kathleen Bowers, Grace M. Kroner, Drew Payto, and Jessica Colon Franco. "Cross-Method Comparison of Serum Androstenedione Measurement Using Three Different Assays: The Siemens Immulite Immunoassay, the Roche Elecsys Immunoassay, and an LC/MS-MS Assay." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A730—A731. http://dx.doi.org/10.1210/jendso/bvab048.1486.
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Abstract Introduction: Androstenedione is a common precursor of male and female sex hormones produced by the adrenal glands and gonads. Serum androstenedione is a helpful biomarker in the diagnostic workup of a subset of patients with polycystic ovary syndrome (PCOS), the investigation of virilizing endocrinopathies, and for monitoring pediatric patients with congenital adrenal hyperplasia. The gold standard for the measurement of androstenedione is LC-MS/MS. A newly developed androstenedione competitive immunoassay is now available in the US, the Roche Elecsys Androstenedione (ASD) immunoassay. Until recently, the Siemens Immulite assay was the only non-radioimmunologic immunoassay available. We characterized the analytical and clinical performance of the ASD across different patient populations and in comparison to the Immulite and an LC-MS/MS assay. Methods and materials: The experiments performed were: linearity and analytical measuring range (AMR), precision (intra- and inter-assay), and accuracy. Androstenedione was measured on de-identified residual serum samples (n=40) using the ASD and Immulite immunoassays and an LC-MS/MS assay. The reference intervals (RIs) provided by Roche for healthy male (0.280-1.52 ng/mL), healthy female (0.490-1.31 ng/mL), postmenopausal women (0.187-1.07 ng/mL), healthy children (<0.519 ng/mL), and patients with PCOS (0.645-3.47 ng/mL) were verified with at least 20 specimens, according to CLSI C28A3. Statistical analysis was performed using EP Evaluator and R program. Results: The ASD had a linear response across the AMR of 0.3 to 10.0 ng/mL. The inter- and intra-assay coefficients of variation were 4.5% and 2.0% or lower, at concentrations 0.5-6.7 ng/mL, respectively. The ASD and LC-MS/MS assays had a mean bias of -0.0542 ng/mL (-2%), Deming regression of y = 1.000 [0.961; 1.039] x - 0.0548 [-0.1806; 0.0709], and r = 0.9930. The Immulite assay had a mean bias of 1.15 ng/mL (44%) and 1.22 ng/mL (32%) compared to the LC-MS/MS and ASD assays, respectively. The recommended RIs from Roche for healthy male, female, and postmenopausal female groups were successfully verified in our patient population. However, the androstenedione concentrations for the healthy children and PCOS groups were outside of the suggested RIs, with concentrations up to 1.41 ng/mL and 0.527-2.24 ng/mL, respectively. Unlike published elsewhere, hormone therapies such as contraceptive pills and steroid treatments did not significantly affect serum androstenedione concentrations in healthy females and patients with PCOS. Conclusion: The ASD is superior to the Immulite immunoassay, and it has excellent comparability with the LC-MS/MS for serum androstenedione measurement. The RIs published by Roche may not be universally transferable; verification is recommended, and establishing RIs for the pediatric population may be necessary.
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Ginther, O. J., E. L. Gastal, M. O. Gastal, and M. A. Beg. "In vivo effects of pregnancy-associated plasma protein-A, activin-A and vascular endothelial growth factor on other follicular-fluid factors during follicle deviation in mares." Reproduction 129, no. 4 (April 2005): 489–96. http://dx.doi.org/10.1530/rep.1.00555.
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During a follicular wave in mares, the two largest follicles (F1 and F2) begin to deviate in diameter when F1 is a mean of 22.5 mm. The intrafollicular effects of pregnancy-associated plasma protein-A (PAPP-A), IGF-I, activin-A and vascular endothelial growth factor (VEGF) on other follicular-fluid factors during deviation were studied. In four treated groups (n= 7/group), a single dose of one of the four factors was injected into F2 when F1 was ≥20.0 mm (expected beginning of deviation). In a control group (n= 7), F2 was injected with vehicle. One day after treatment, a sample of follicular fluid was taken from F1 and F2 of the control group and from F2 of the treated groups and was assayed for free IGF-I, oestradiol, androstenedione, activin-A, inhibin-A, follistatin and VEGF. In the control group, the means for all end points were significantly greater in F1 than in F2, except that concentrations of androstenedione were lower in F1 than in F2. The treatment effects for F2 were significant as follows: PAPP-A increased the concentrations of free IGF-I, inhibin-A, follistatin and VEGF and decreased the concentrations of androstenedione; IGF-I increased the concentration of inhibin-A and decreased the concentration of androstenedione; activin-A decreased the concentrations of follistatin and androstenedione and increased the diameter of F2; and VEGF increased the concentration of IGF-I and decreased the concentration of androstenedione. These results support the hypotheses that during deviation in mares PAPP-A increases the follicular-fluid concentrations of free IGF-I, follistatin responds to changes in follicular-fluid concentrations of activin-A, and VEGF affects the concentrations of other follicular-fluid factors.
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Provencher, P. H., Y. Tremblay, and A. Bélanger. "Effects of C19 steroids on adrenal steroidogenic enzyme activities and their mRNA levels in guinea-pig fasciculata-glomerulosa cells in primary culture." Journal of Endocrinology 132, no. 2 (February 1992): 269–76. http://dx.doi.org/10.1677/joe.0.1320269.
Full textAbstract:
ABSTRACT The present study examined the effects of steroids on steroidogenic enzyme activity in adrenal glands. Guinea-pig fasciculata-glomerulosa (FG) cells maintained in primary culture were exposed to steroids for 48 h. Although the treatment with androstenedione alone had no effect on 3β-hydroxysteroid dehydrogenase 4-ene-5-ene-isomerase (3β-HSD), 17-hydroxylase and 17,20-lyase activities, there was inhibition of 11-hydroxylase and 21-hydroxylase activities. When FG cells were exposed to 10 nmol ACTH/l for the last 24 h of incubation, ACTH alone had no effect on steroidogenic enzymes but, while combined with androstenedione, it further decreased 21-hydroxylase activity and stimulated 17-hydroxylase and 17,20-lyase activities. Cortisol, corticosterone, oestradiol and 11β-hydroxy androstenedione had no effect on steroidogenic enzyme activities while the inhibitory effect on 21-hydroxylase activity was only observed with androstenedione, testosterone and dihydrotestosterone. Addition of hydroxyflutamide, a pure antiandrogen, did not block the inhibitory effect of androstenedione on 21-hydroxylase and 11-hydroxylase activities. The reduction in oxygen tension from 19 to 2% which was aimed at examining the oxygen-mediated effects on steroidogenic enzymes, revealed that the reduction in 21-hydroxylase activity induced by androstenedione could not be prevented by low oxygen tension. An interaction of C19 steroids at the level of the enzymes is also suggested by our finding that androstenedione had no effect on basal and ACTH-stimulated steady-state 11-hydroxylase, 17-hydroxylase, 17,20-lyase and 21-hydroxylase mRNA levels. These results indicate that C19 steroids alter the adrenal steroidogenic enzyme activities in such a manner that C19 steroid synthesis is increased while glucocorticoid production is inhibited. The mechanism of action of C19 steroids does not involve gene expression for steroidogenic enzymes but probably a direct interaction with steroidogenic enzymes, namely 21-hydroxylase, 17-hydroxylase and 17,20-lyase. Our data suggest that C19 steroids may reduce the amount of 21-hydroxylase in the microsomal fraction which may have a major impact on the levels of microsomal P450 reductase available for 17-hydroxylase and 17,20-lyase activities. Journal of Endocrinology (1992) 132, 269–276
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Büttler, Rahel M., Frans Martens, Flaminia Fanelli, Hai T. Pham, Mark M. Kushnir, Marcel J. W. Janssen, Laura Owen, et al. "Comparison of 7 Published LC-MS/MS Methods for the Simultaneous Measurement of Testosterone, Androstenedione, and Dehydroepiandrosterone in Serum." Clinical Chemistry 61, no. 12 (December 1, 2015): 1475–83. http://dx.doi.org/10.1373/clinchem.2015.242859.
Full textAbstract:
Abstract BACKGROUND Recently, LC-MS/MS was stated to be the method of choice to measure sex steroids. Because information on the mutual agreement of LC-MS/MS methods is scarce, we compared 7 published LC-MS/MS methods for the simultaneous measurement of testosterone, androstenedione, and dehydroepiandrosterone (DHEA). METHODS We used 7 published LC-MS/MS methods to analyze in duplicate 55 random samples from both men and women. We performed Passing–Bablok regression analysis and calculated Pearson correlation coefficients to assess the agreement of the methods investigated with the median concentration measured by all methods, and we calculated the intraassay CV of each method derived from duplicate results and the CVs between the methods. RESULTS Median concentrations of testosterone were 0.22–1.36 nmol/L for women and 8.27–27.98 nmol/L for men. Androstenedione and DHEA concentrations were 0.05–5.53 and 0.58–18.04 nmol/L, respectively. Intraassay CVs were 2.9%–10%, 1.2%–8.8%, 2.7%–13%, and 4.3%–16% for testosterone in women, testosterone in men, androstenedione, and DHEA. Slopes of the regression lines calculated by Passing–Bablok regression analysis were 0.92–1.08, 0.92–1.08, 0.90–1.13, and 0.91–1.41 for all testosterone values, testosterone in women, androstenedione, and DHEA. Intermethod CVs were 14%, 8%, 30%, and 22% for testosterone in women, testosterone in men, androstenedione, and DHEA. CONCLUSIONS In general, the LC-MS/MS methods investigated show reasonable agreement. However, some of the assays show differences in standardization, and others show high variation.
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Wrathall, J. H. M., and P. G. Knight. "Effects of inhibin-related peptides and oestradiol on androstenedione and progesterone secretion by bovine theca cells in vitro." Journal of Endocrinology 145, no. 3 (June 1995): 491–500. http://dx.doi.org/10.1677/joe.0.1450491.
Full textAbstract:
Abstract Primary monolayer cultures of bovine theca cells isolated from pooled ovarian follicles (3–10 mm diameter) were used to examine the effects of various granulosa cell-derived substances on basal and luteinizing hormone (LH)-induced androgen and progesterone secretion. After an overnight pretreatment period, cells were incubated with a range of treatments including LH, oestradiol-17β, inhibin, activin and follistatin. Media were collected after 48 h and assessment of androstenedione and progesterone secretion made by radioimmunoassay. Addition of LH (5–50 ng/ml) to the cells resulted in a dose-dependent stimulation of both androstenedione (2·5-to 3-fold rise; P<0·01) and progesterone (∼ 1·6-fold rise; P<0·001) production. Secretion of androstenedione was also raised (up to 5-fold; P<0·001) by addition of oestradiol-17β (0·3–300 ng/ml), whilst levels of the androgen in the presence of both LH (20 ng/ml) and oestradiol (300 ng/ml) were up to 12-fold higher (P<0·001) than control values. In contrast, oestradiol treatment inhibited by up to 50% both basal (P<0·001) and LH-stimulated (P<0·001) secretion of progesterone. Exposure of cells to purified bovine inhibin (5–125 ng/ml) consistently raised androstenedione secretion by up to 42% over basal levels (P<0·001). Inhibin also enhanced both LH-stimulated (∼20%; P<0·001) and oestradiol-stimulated (∼20%; P<0·05) secretion of androstenedione. In direct contrast, treatment of theca cells with human recombinant activin-A (1–50 ng/ml) inhibited both LH-stimulated (∼50%; P<0·001) and oestradiol-stimulated (∼30%; P<0·005) androstenedione secretion. Activin also reversed the positive effect of inhibin on basal (P<0·01), LH-stimulated (P<0·001) and oestradiol-stimulated (P<0·001) androstenedione secretion, though activin alone did not affect basal steroid output. Simultaneous addition of human recombinant follistatin reversed the inhibitory effects of activin on LH- and oestradiol-induced androstenedione secretion but did not modify the effects of inhibin. Follistatin alone did not alter either basal or LH-stimulated androstenedione output. Neither basal nor LH-stimulated secretion of progesterone were consistently affected by inhibin, activin or follistatin. As well as confirming the stimulatory effects of both LH and oestradiol on bovine thecal cell androgen production, these observations are indicative of opposing intrafollicular paracrine roles for granulosa cell-derived inhibin and activin in modulating thecal cell responses to gonadotrophins and steroids in the bovine ovary. Though inhibin and oestradiol had qualitatively similar effects in promoting thecal androgen secretion, the magnitude of the response to oestradiol was much greater. The results also support an intrafollicular role of follistatin as a binding protein capable of neutralizing the effect of activin, but not inhibin, on thecal androgen production. Journal of Endocrinology (1995) 145, 491–500