Effects of 17β-estradiol on pituitary and testicular function in male goldfish

1993 ◽  
Vol 71 (6) ◽  
pp. 1131-1135 ◽  
Author(s):  
V. L. Trudeau ◽  
M. G. Wade ◽  
G. Van Der Kraak ◽  
R. E Peter

The potential involvement of 17β-estradiol in the regulation of pituitary and testicular function was investigated in male goldfish at various times during the seasonal reproductive cycle. Serum levels of testosterone, 11-ketotestosterone, and 17β-estradiol were 10, 16, and 4 times higher in mature males (tubercles on the pectoral fins and milt production; March) than in sexually regressed males (no tubercles or milt production; July). Intraperitoneal injection of [D-Arg6,Trp7,Leu8,Pro9-NEt]gonadotropin releasing hormone (sGnRH-A, 0.01 μg/g) elevated serum gonadotropin II levels within 6 h, and there was a concomitant increase in testosterone but not 17β-estradiol levels in sexually regressing male goldfish (October). Males in the early stage of testicular recrudescence (November) had increased serum levels of gonadotropin II and testosterone in response to [D-Ala6,Pro9-NEt]GnRH (LHRH-A, 0.1 μg/g) or the dopamine antagonist domperidone (5 μg/g). Males implanted intraperitoneally for 10 days with solid Silastic pellet implants containing 17β-estradiol (100 μg/g) had lower basal testosterone levels and a reduced testosterone response to both LHRH-A and domperidone. The serum gonadotropin II response to LHRH-A but not domperidone was enhanced by 17β-estradiol. Male goldfish in mid-recrudescence receiving 17β-estradiol implants for 4 days had lower basal testosterone and 11-ketotestosterone levels than controls. Combined treatment with sGnRH-A (0.1 μg/g) and domperidone (10 μg/g) elevated serum testosterone and 11-ketotestosterone levels at 24 h; the serum androgen response was reduced in 17β-estradiol-implanted fish. These studies support the concept that 17β-estradiol plays a role in the regulation of reproduction in male goldfish by enhancing pituitary gonadotropin II release and by reducing testicular androgen production.

PEDIATRICS ◽  
1983 ◽  
Vol 72 (3) ◽  
pp. 384-389
Author(s):  
Harold K. Marder ◽  
Laxmi S. Srivastava ◽  
Stephen Burstein

Serum gonadotropin and testosterone concentrations were measured in ten peripubertal boys to assess the effects of uremia on pubertal maturation. Serum luteinizing hormone (LH) concentrations were elevated for stage of puberty in eight boys, whereas in most boys serum follicle-stimulating hormone and testosterone concentrations were normal. Serum LH concentrations correlated with the severity of uremia. LH levels declined when measured 1 year after the initial measurements in four boys who received renal allografts, but were further elevated in two boys who were treated conservatively. Elevated serum LH concentrations in the presence of normal serum testosterone concentrations imply limited testicular sensitivity to the effects of LH in these peripubertal boys, as has been documented for adult men with chronic renal failure. Alternatively, there may be accumulation of an immunoreactive LH molecule that lacks bioactivity. A testicular dysfunction may explain the pubertal delay experienced by some uremic adolescent boys.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 740-740
Author(s):  
YOSHIKAZU NISHI ◽  
SHUICHI HATANO ◽  
KATSUAKI AIHARA ◽  
TOMOFUSA USUI

To the Editor.— We read with great interest the paper of Marder et al1 on hypergonadotropism in peripubertal boys with chronic renal failure. However, their discussion does not mention the role of zinc in testicular function. Zinc deficiency not only reduces zinc levels in the reproductive tissues but also impairs the responsiveness of the Leydig cells to gonadotropins, and thus may cause primary hypogonadism in humans as well as in experimental animals.2-4 Moreover, testicular hypofunction, elevated serum gonadotropin levels, and subnormal plasma zinc levels have been reported in renal failure.5,6


Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 881
Author(s):  
Zhao Zhang ◽  
Guorong Zhang ◽  
Meng Guo ◽  
Wanyin Tao ◽  
Xingzi Liu ◽  
...  

The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global concern. Immunoglobin A (IgA) contributes to virus neutralization at the early stage of infection. Longitudinal studies are needed to assess whether SARS-CoV-2-specific IgA production persists for a longer time in patients recovered from severe COVID-19 and its lasting symptoms that can have disabling consequences should also be alerted to susceptible hosts. Here, we tracked the anti-SARS-CoV-2 spike protein receptor-binding domain (RBD) antibody levels in a cohort of 88 COVID-19 patients. We found that 52.3% of the patients produced more anti-SARS-CoV-2 RBD IgA than IgG or IgM, and the levels of IgA remained stable during 4–41 days of infection. One of these IgA-dominant COVID-19 patients, concurrently with IgA nephropathy (IgAN), presented with elevated serum creatinine and worse proteinuria during the infection, which continued until seven months post-infection. The serum levels of anti-SARS-CoV-2 RBD and total IgA were higher in this patient than in healthy controls. Changes in the composition of the intestinal microbiota, increased IgA highly coated bacteria, and elevated concentration of the proinflammatory cytokine IL-18 were indicative of potential involvement of intestinal dysbiosis and inflammation to the systemic IgA level and, consequently, the disease progression. Collectively, our work highlighted the potential adverse effect of the mucosal immune response to SARS-CoV-2 infection, and that additional care should be taken with COVID-19 patients presenting with chronic diseases such as IgAN.


2018 ◽  
Vol 107 (2) ◽  
pp. 105-113 ◽  
Author(s):  
Ali Abbara ◽  
Sophie A. Clarke ◽  
Alexander Nesbitt ◽  
Sabreen Ali ◽  
Alexander N. Comninos ◽  
...  

Background/Aims: Hyperprolactinaemia is a common cause of amenorrhoea due to hypogonadotropic hypogonadism. Prolactin is hypothesised to impede the reproductive axis through an inhibitory action at the hypothalamus. However, limited data exist to aid the interpretation of serum gonadotropins in the context of hyperprolactinaemia. Methods: Serum gonadotropin values were reviewed in 243 patients with elevated serum monomeric prolactin due to discrete aetiologies at a tertiary reproductive endocrine centre between 2012 and 2015. The cause of hyperprolactinaemia was categorised by an experienced endocrinologist/pituitary multidisciplinary team, unless superseded by histology. The most frequently encountered diagnoses were microprolactinoma (n = 88), macroprolactinoma (n = 46), non-functioning pituitary adenoma (NFPA) (n = 72), drug-induced hyperprolactinaemia (n = 22) and polycystic ovarian syndrome (PCOS) (n = 15). Results: In patients with prolactinoma and modestly raised serum prolactin levels (< 4,000 mU/L), increasingly FSH-predominant gonadotropin values were observed with rising prolactin level, consistent with a progressive reduction in hypothalamic gonadotropin-releasing hormone (GnRH) pulsatility. Patients with prolactinoma and higher prolactin values (> 4,000 mU/L) were more likely to have a reduction in serum levels of both FSH and LH, consistent with direct pituitary gonadotrope dysfunction. Patients with macroadenoma and extremes of serum gonadotropin values (either serum FSH or LH > 8 IU/L) were more likely to have NFPA than prolactinoma. Patients with PCOS and hyperprolactinaemia had LH-predominant secretion in keeping with increased GnRH pulsatility despite a raised prolactin level. Conclusion: The pattern of gonadotropin secretion in patients with hyperprolactinaemia reflects the underlying aetiology.


2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Eek Chaw Tan ◽  
Chit Chong Khong ◽  
Kazila Bhutia

Steroid cell tumour is a rare sex cord-stromal tumor of the ovary. It may produce steroids and is associated with testosterone secretion which causes symptoms like hair loss, hirsutism, and oligomenorrhea/amenorrhea due to hormonal activity and virilizing properties of tumor. In this article, we reported a 27-year-old woman who presented with hirsutism, hoarseness of voice, scalp hair fall, and amenorrhea for 8 years. Clinical and diagnostic evaluation revealed a left adnexal mass and elevated serum levels of testosterone and she was diagnosed as having a Sertoli Leydig cell tumour of ovary. She underwent left salpingooophorectomy and both histopathological examination and immunohistochemistry confirmed the diagnosis. Her serum testosterone levels normalized 3 days after the surgery and her menses resumed spontaneously a few months after the operation. In addition, we reviewed the literature on the epidemiology, clinical presentations, imaging and histological findings, and the treatment options on this disease.


BioMedicine ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 24 ◽  
Author(s):  
Yasser Mohamed ◽  
Mohamed A. Basyony ◽  
Nabila I. El-Desouki ◽  
Walied S. Abdo ◽  
Mohammed A. El-Magd

Background/aim: Herein, we investigated the potential therapeutic effect of Melatonin (Mel) and/or mesenchymal stem cells (MSCs) on rat model of HCC. Materials and Methods: Female mature rats were divided into 5 groups (n = 10/group): normal (Nor), HCC group intraperitoneally injected with 200 mg/kg DEN, and 3 treated groups; HCC + Mel (Mel) group given Mel intraperitoneally 20 mg/kg, twice a week, HCC + MSCs (MSCs) group intravenously injected by 1 × 106 cells, and HCC + MSCs (Mel +MSCs) group. Results: Rats in HCC group showed most deteriorated effect in form of increased mortality and relative liver weight, elevated serum levels of ALT, AST, ALP, AFP and GGT in addition to increased pre-neoplastic nodules in liver tissues. Liver tissues of HCC group also exhibited lower level of apoptosis as indicated by decreased DNA fragmentation and expression of p53 caspase 9 and caspase 3 genes and increased PCNA immunoreactivity. Moreover, in this group the expression of IL6 and TGFβ1 genes was significantly upregulated. All these deleterious effects induced by DEN were reversed after administration of Mel and/ or MSCs with best improvement for the combined group (MSCs + Mel). Conclusions: These findings reveal a better therapeutic effect for MSCs when given with Mel and we attribute this beneficial effect, at least in part, to triggering apoptosis and targeting inflammation in HCC. Therefore, combined treatment with Mel and MSCs is recommended to enhance the therapeutic potential against HCC.


2020 ◽  
Author(s):  
Gertjan Vereecke ◽  
Justine Defreyne ◽  
Dorien Van Saen ◽  
Sarah Collet ◽  
Jo Van Dorpe ◽  
...  

Abstract STUDY QUESTION Does gender-affirming treatment prevent full spermatogenesis in transgender women (TW)? SUMMARY ANSWER Adequate hormonal therapy (HT) leads to complete suppression of spermatogenesis in most TW, if serum testosterone levels within female reference ranges are obtained. WHAT IS KNOWN ALREADY Gender-affirming treatment in transgender individuals may involve gender-affirming HT. The effects on spermatogenesis in TW remain unclear. In order to add information from a referral centre for transgender care, we wish to compare results of earlier studies with our population of TW who received a standard hormone treatment. STUDY DESIGN, SIZE, DURATION This was a prospective cohort study part of the European Network for the Investigation of Gender Incongruence (ENIGI), conducted between 15 February 2010 and 30 September 2015. There were 162 TW were included in the ENIGI study at the Ghent University Hospital in Belgium. Participants are included in ENIGI when they first start HT, and follow-up visits occur over the next 3 years. PARTICIPANTS/MATERIALS, SETTING METHODS The study included 97 TW who initiated HT with cyproterone acetate (CPA) plus oestrogens and proceeded with gonadectomy at the Ghent University Hospital. Testicular tissue retrieved during gonadectomy was processed and stained for four different germ cell markers by the Biology of the Testis lab at the Vrije Universiteit Brussel. Subsequent immunohistochemical staining was performed for melanoma-associated antigen A4 (MAGE-A4, marker for spermatogonia and early spermatocytes), boule homologue, RNA-binding protein (BOLL, marker for secondary spermatocytes and round spermatids), cAMP-responsive element modulator (CREM, marker for round spermatids) and acrosin (marker for acrosome visualization). Serum levels of sex steroids were measured prior to surgery. MAIN RESULTS AND THE ROLE OF CHANCE Suppressed testosterone levels (&lt;50 ng/dl) were found in 92% of the participants prior to surgery. The mean time between initiation of HT and surgery was 685 days. In 88% (85/97) of the sections, MAGE-A4 staining was positive. Further staining could not reveal complete spermatogenesis in any participant. LIMITATIONS, REASONS FOR CAUTION Testicular function of the participants prior to initiation of HT was not assessed, although all participants presented with cisgender male serum testosterone values before initiation of HT. The current study only reports on people using CPA at a fixed dose and may therefore not be applicable to all TW. WIDER IMPLICATIONS OF THE FINDINGS HT leads to complete suppression of spermatogenesis in most TW, if serum testosterone levels within female reference ranges are obtained. Serum testosterone levels are associated with the sperm maturation rate. It is important to discuss sperm preservation before the start of hormone therapy. If serum testosterone levels remain higher, spermatogenesis may still occur. STUDY FUNDING/COMPETING INTEREST(S) D.V.S. is a post-doctoral fellow of the Fonds Wetenschappelijk Onderzoek (FWO; 12M2819N). Processing of the testis specimens was funded by the Biology of The Testes (BITE) research group (Department of Reproduction, Genetics and Regenerative medicine at Vrije Universiteit Brussel (VUB)). There are no competing interests. TRIAL REGISTRATION NUMBER N/A.


1991 ◽  
Vol 69 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Frank H. Yu ◽  
Young W. Yun ◽  
Basil Ho Yuen ◽  
Young S. Moon

Immature female rats treated with superovulatory doses of pregnant mare serum gonadotropin (PMSG) were used to study the effects of the antiandrogen hydroxyflutamide on steroid production, particularly the biologically active androgens, in two experiments. In the first experiment, animals were given either 5 mg hydroxyflutamide or vehicle alone at 30 and 36 h following 40 IU PMSG. Compared with the vehicle group, hydroxyflutamide treatment significantly reduced the percentage of degenerate oocytes recovered from oviducts (p < 0.05). Serum levels of testosterone and androstenedione, and their aromatized product 17β-estradiol, significantly decreased (p < 0.05) in the hydroxyflutamide-treated group; however, nonaromatizable androgen, 5α-dihydrotestosterone, was not affected. In the second experiment, ovaries obtained 48 h after stimulation with 4 or 40 IU PMSG were incubated with and without hydroxyflutamide (10−5 M) and (or) testosterone (10−7 M) to study [4-14C]pregnenolone metabolism to major steroids. In 40 IU stimulated ovaries, hydroxyflutamide significantly decreased the metabolism of pregnenolone to progesterone (p < 0.01) and androstenedione (p < 0.01), while the production of 17β-estradiol increased significantly (p < 0.05); however, pregnenolone conversions to testosterone and 5α-dihydrotestosterone were not affected. Testosterone completely reversed the hydroxyflutamide-induced alteration of pregnenolone metabolism. In contrast, there was no difference in the pregnenolone conversion patterns between untreated and hydroxyflutamide or hydroxyflutamide plus testosterone groups in 4 IU stimulated ovaries. Present results confirm our previous finding that hydroxyflutamide decreases the percentage of abnormal oocytes recovered from superovulating rats and indicates that this hydroxyflutamide effect may be partly mediated by altered ovarian steroidogenesis following inhibition of androgen binding in the ovary.Key words: superovulation, pregnant mare serum gonadotropin, antiandrogen, hydroxyflutamide, androgen.


1979 ◽  
Vol 92 (3) ◽  
pp. 532-541 ◽  
Author(s):  
Nobuaki Furuhashi ◽  
Victor S. Fang

ABSTRACT The relationship between serum levels of growth hormone (rGH), prolactin (rPRL), lutenizing hormone (rLH), follicle-stimulating hormone (rFSH), corticosterone, oestrogen, (oestradiol-17β) and testosterone and the hepatic binding sites specific to [125I]human-prolactin (h-PRL) were investigated in normal rats, in rats bearing the GH- and PRL-secreting tumour (GH3), and in rats 14 days after tumour removal. The presence of GH3 tumour elevated serum levels of rGH and rPRL and concomitantly increased the hepatic binding of [125I] h-PRL; the male rats had a greater increase than the female rats. The increased binding was due to an increase in the specific membrane binding sites, whereas the affinity constant (Ka) was not changed. In both male and female rats, there was a significant positive correlation between serum rGH levels (P < 0.001) or serum rPRL (P < 0.02) and specific binding of [1251] h-PRL in female rats only (P < 0.02). In male rats, there was a significant negative correlation between serum testosterone levels and specific bindings of [125I]h-PRL (P < 0.05). These results suggest that rGH and rPRL regulates the hepatic h-PRL receptors in female rats, and testosterone predominantly inhibits the induction of the hepatic lactogenic receptors in male rats.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cleo C. L. van Aanhold ◽  
Manon Bos ◽  
Katrina M. Mirabito Colafella ◽  
Marie-Louise P. van der Hoorn ◽  
Ron Wolterbeek ◽  
...  

AbstractThe endothelial glycoprotein thrombomodulin regulates coagulation, vascular inflammation and apoptosis. In the kidney, thrombomodulin protects the glomerular filtration barrier by eliciting crosstalk between the glomerular endothelium and podocytes. Several glomerular pathologies are characterized by a loss of glomerular thrombomodulin. In women with pre-eclampsia, serum levels of soluble thrombomodulin are increased, possibly reflecting a loss from the glomerular endothelium. We set out to investigate whether thrombomodulin expression is decreased in the kidneys of women with pre-eclampsia and rats exposed to an angiogenesis inhibitor. Thrombomodulin expression was examined using immunohistochemistry and qPCR in renal autopsy tissues collected from 11 pre-eclamptic women, 22 pregnant controls and 11 hypertensive non-pregnant women. Further, kidneys from rats treated with increasing doses of sunitinib or sunitinib in combination with endothelin receptor antagonists were studied. Glomerular thrombomodulin protein levels were increased in the kidneys of women with pre-eclampsia. In parallel, in rats exposed to sunitinib, glomerular thrombomodulin was upregulated in a dose-dependent manner, and the upregulation of glomerular thrombomodulin preceded the onset of histopathological changes. Selective ETAR blockade, but not dual ETA/BR blockade, normalised the sunitinib-induced increase in thrombomodulin expression and albuminuria. We propose that glomerular thrombomodulin expression increases at an early stage of renal damage induced by antiangiogenic conditions. The upregulation of this nephroprotective protein in glomerular endothelial cells might serve as a mechanism to protect the glomerular filtration barrier in pre-eclampsia.


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