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Expression of estrogen receptors α and β in paratesticular tissues in boys operated on for unilateral cryptorchidism between the 1st and 4th years of life.
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PMID:  23018357     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: The aim of this study was to assess the expression of estrogen receptors alpha and beta in paratesticular tissues in a group of boys with and without cryptorchidism, and evaluation of karyotypes, localization, morphology and the major length of the undescended testes.
MATERIAL/METHODS: Fifty boys (1-4 years old) with unilateral cryptorchidism were evaluated. Fifty healthy boys within the same age range, with inguinal hernia, served as a control group. Measurements concerning expression of ERalpha ERbeta receptors were preformed using monoclonal mouse antibodies against human receptor alpha and beta.
RESULTS: In the mesothelial layer, the expression of ERalpha was higher in the patients group with undescended testes and it was statistically significant (p=0.04). There was no difference in the expression of ERbeta in this layer between groups. In the stromal cell layer there was statistically significant higher expression of ERbeta (p<0.05) in the group of patients with undescended testes.
CONCLUSIONS: There was no difference between expressions of ERalpha in stromal cell layer. In the endothelial layer there was no difference in expression of ERalpha and ERbeta. In the smooth muscle layer there was no expression of ERalpha in either group. The expression of ERbeta in the smooth muscle layer was nearly identical in both groups. Undescended testes were generally found in the superficial inguinal pouch (n=46). The major lengths of the undescended testes were smaller in comparison to the testes positioned normally. In 9 of the cases the testes had different shape, and turgor deficit, and epididymides were smaller, dysplastic and separated from the testis.
Adam Hermanowicz; Ewa Matuszczak; Wojciech Debek; Ewa Dzienis-Koronkiewicz; Marta Komarowska; Marzanna Oksiuta; Jolanta Kowalewska; Robert Milewski
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Medical science monitor : international medical journal of experimental and clinical research     Volume:  18     ISSN:  1643-3750     ISO Abbreviation:  Med. Sci. Monit.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-28     Completed Date:  2013-02-19     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  9609063     Medline TA:  Med Sci Monit     Country:  Poland    
Other Details:
Languages:  eng     Pagination:  CR630-4     Citation Subset:  IM    
Department of Pediatric Surgery Medical University of Bialystok, Bialystok, Poland.
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MeSH Terms
Child, Preschool
Cryptorchidism / metabolism*,  pathology,  surgery*
Estrogen Receptor alpha / metabolism*
Estrogen Receptor beta / metabolism*
Testis / metabolism*,  pathology
Reg. No./Substance:
0/Estrogen Receptor alpha; 0/Estrogen Receptor beta; 0/estrogen receptor alpha, human

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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Journal Information
Journal ID (nlm-ta): Med Sci Monit
Journal ID (iso-abbrev): Med. Sci. Monit
Journal ID (publisher-id): Medical Science Monitor
ISSN: 1234-1010
ISSN: 1643-3750
Publisher: International Scientific Literature, Inc.
Article Information
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© Med Sci Monit, 2012
Received Day: 06 Month: 2 Year: 2012
Accepted Day: 13 Month: 6 Year: 2012
collection publication date: Year: 2012
Electronic publication date: Day: 01 Month: 10 Year: 2012
Volume: 18 Issue: 10
First Page: CR630 Last Page: CR634
PubMed Id: 23018357
ID: 3560562
Publisher Id: 883490

Expression of estrogen receptors α and β in paratesticular tissues in boys operated on for unilateral cryptorchidism between the 1st and 4th years of life
Adam Hermanowicz1ABDEF
Ewa Matuszczak1BEF
Wojciech Debek1BDE
Ewa Dzienis-Koronkiewicz1B
Marta Komarowska1BFE
Marzanna Oksiuta1B
Jolanta Kowalewska2CE
Robert Milewski3C
1Department of Pediatric Surgery Medical University of Bialystok, Bialystok, Poland
2Department of Medical Pathomorphology Medical University of Bialystok, Bialystok, Poland
3Department of Statistics and Medical Informatics Medical University of Bialystok, Bialystok, Poland
Correspondence: Adam Hermanowicz, Department of Pediatric Surgery Medical University of Bialystok, Waszyngtona 17 St., 15-274 Bialystok, Poland, e-mail:
AStudy Design
BData Collection
CStatistical Analysis
DData Interpretation
EManuscript Preparation
FLiterature Search
GFunds Collection


There is growing evidence from clinical and epidemiological studies for an increasing incidence of male reproductive disorders (ie, cryptorchidism). The etiology of undescended testis is still surrounded by much controversy. Approximately 90% of cases of cryptorchidism occur spontaneously or from unknown causes. The process of descending of the testes is one of the most important factors in spermatogenesis in mature testis. This suggests that environmental or lifestyle, rather than genetic, factors are plausible causes [1]. Indeed, mutations in the Insl3 or LGR8 loci do not seem to represent a frequent cause of human cryptorchidism [2].

A broad expression of estrogen receptors (ERs) in the testis suggests an important role of estrogens in regulating testicular cell function and reproductive events. Estrogen is a key regulator of growth and differentiation in a broad range of target tissues – the reproductive tract, mammary gland, and the central nervous and skeletal systems [3,4]. Estrogen is also known to be involved in many pathological processes such as breast and endometrial cancer, and osteoporosis [5,6]. The major source of endogenous estrogen in men is adipose tissue, but the receptor proteins (ERα and ERβ) are localized in most cell types in the testis in concordance with a physiological role for estrogen in testicular development and function [7]. The presence of an estrogen binding receptor protein – ERα – was first reported in 1962 [8]. In 1996, an additional estrogen receptor – ERβ – was cloned from rat prostate [9]. ERβ were cloned from many species, including humans [10,11]. ERα and ERβ belong to the superfamily of nuclear receptors and specifically to the family of steroid receptors that act as ligand-regulated transcription factors [12,13]. ERα and ERβ have different biological functions and different phenotypes [14]. Abnormal estrogen action has been implicated as a possible cause for sporadic cryptorchidism in humans [15]. Animal studies support the human correlations. In mice, in utero exposure to estradiol induces cryptorchidism [1619]. Estradiol is known to inhibit androgen production, either by limiting the development and growth of Leydig cells, or by directly inhibiting the activities of several steroidogenic enzymes involved in testosterone synthesis [20]. Estradiol is produced not only by the mother, but also in significant amounts by Sertoli cells [21,22]. In addition, testes concentrate estradiol as much as 10- to 50-fold higher than in peripheral blood [23]. Despite the above facts, the intra-abdominal position of the testes in estrogen-treated mice is due to the absence of Insl3 hormone, but not of androgens. Estrogens block the first phase of testicular descent (transabdominal descent), whereas androgens control only the second, inguinoscrotal, phase [2426]. The first phase of typical testicular descent takes place between the 10th and 15th weeks of human gestation [27]. This occurrence is independent of androgen levels, as the process has been found to transpire in both animals and humans with complete androgen insensitivity, and is believed to be influenced by AMH (anti-Müllerian hormone) and insulin-like hormone 3 (INSL3) [28,29]. INSL3 is secreted by Leydig cells shortly after the onset of testicular development, and controls the thickening of the gubernaculum anchoring the testis to the inguinal region [30]. Disruption of the INSL3 gene in mice results in bilateral intra-abdominal testes [25,31]. In humans, it was found that only 1.9% of the cases of cryptorchidism were caused by INSL3 gene mutations, and that the mutations of the INSL3 receptor on the whole were uncommon [32,33]. The second, or inguinoscrotal, phase of testicular descent occurs between the 26th to 40th weeks of gestation [27]. During this phase, the testes migrate through the inguinal canal and across the pubic region to the scrotum. The testis and epididymis then remain within the diverticulum of the peritoneum, which elongates within the gubernaculum [34]. Furthermore, the gubernaculum, growing out of the abdominal wall, might be under the control of Hox genes – a group of genes that determines the basic structure and orientation of an organism. Disruption of some Hox genes in mice has been shown to lead to cryptorchidism, but the relevance of this observation is debatable in human studies of cryptorchidism [35]. On the other hand, there is much clinical evidence that shows reduced androgen action to be associated with undescended testes [36].

In the present study we assessed expression of estrogen receptors α and β in paratesticular tissues in a group of boys with and without cryptorchidism. We evaluated the karyotypes of these boys, as well as the position, morphology and diameters of the undescended testes.

Material and Methods
Study population

Fifty boys aged 1–4 years (median=2,4 y.) with unilateral cryptorchidism, and without previous human chorionic gonadotropin treatment, were evaluated. All of them underwent orchidopexy in 2010. Abnormal karyotype, as well as the presence of any endocrine disorders, and hormonal drugs intake, constituted grounds for exclusion from the study. Prior to their orchidopexy, all of the subjects had their karyotypes (to exclude chromosomal abnormalities) evaluated. During the actual orchidopexy, the gubernaculum samples were collected, the position and morphology of the testes were evaluated, and their diameters were measured.

Control group

Fifty healthy boys aged 1–4 years (median=2,1 y.), admitted to the Pediatric Surgery Department for planned inguinal hernia repairs in 2010, served as controls. All boys in the control group had their testes in the scrotum. Their karyotypes were also determined prior to their procedures. The samples of the diverticulum of the peritoneum were collected during herniotomy.

Data were collected from patients admitted to the Pediatric Surgery Department for either a planned orchidopexy or hernia repair. All parents of the patients gave informed consent for both clinical and histological follow-up. Tissue samples – gubernaculum and diverticulum of peritoneum – were collected during planned surgeries. Measurements of expression of ER α ER β receptors were preformed using monoclonal mouse antibodies against human receptor α, (Monoclonal Mouse Anti-Human Estrogen Receptor α, clone 1D5, of IgG1 kappa isotype), and β (Monoclonal Mouse Anti-Human Estrogen Receptor β clone PPG5/10), respectively. In further stages we used anti-mouse antibody combined with biotin and peroxidase, and visualized by using FLEX+ Mouse, High pH (K8002/K8012) for alpha receptors and DAKO LSAB+/HRP, (K 0679) and DAKO EnVision+/HRP (K4004 and K4006) for beta. Sections were counter-stained with haematoxylin. The results were expressed as the percentage of positive cells with a strong positive receptor staining and labeled as follows: negative (−) with ≤10% of positive cells, positive (+) with 11% to 50% of positive cells, and highly positive (++) with ≥51% positive cells, in a set of 10 random fields under 20× magnification.

The study was approved by the local Ethics Committee as an audit of a clinically agreed-upon protocol of investigation and treatment.

Statistical analyses

Statistical analyses were carried out using Statistica 10.0 StatSoft. To compare observed data we used chi-square test and Pearson’s correlation. P values less than 0.05 were considered significant.


There was no statistically significant difference in the age distribution of the 2 groups. All boys had karyotypes 46XY. The undescended testes were mainly localized in the inguinal canal (n=46), but in 2 of the instances were located in the external ring of the inguinal canal, while 2 more subjects had theirs in the abdominal cavity. The overall lengths of the undescended testes differed from 0.8 cm to 2 cm, and in most cases were found to be smaller in comparison to the testes positioned normally (mean 1 cm and mean 1.5 cm, respectively). In 9 of the cases of cryptorchidism, the testes had different shape (drop-like), and the epididymides were small, dysplastic and separated from the testis.

We measured expression of Erα and ERβ in paratesticular tissues: in the mesothelial layer, stromal cells, endothelial layer, and smooth muscle layer.

In the mesothelial layer there was a statistically significant (p=0.04) difference in the expression of ERα. The expression of ERα was higher in undescended testes. In 71% of the cases of the cryptorchidism we found a high expression of the ERα. In the inguinal hernia group the strong expression (++) were found only in 18% of the cases. We also found that in 32% of the inguinal hernia patients there was no ERα expression at all. There was no difference in the expression of ERβ in the mesothelial layer between the 2 groups.

In the stromal cell layer there was statistically significant higher expression of ERβ (p<0.05) in undescended testes. In these cases, 62% of patients with undescended testes had a strong ERβ expression. There was no statistically significant difference between expressions of ERα in stromal cell layer between the 2 groups.

In the endothelial layer there was no statistically significant difference in expression of ERα and ERβ between the 2 groups. In the both groups, expression of the ERα and ERβ in most of the cases were only positive (+).

In the smooth muscle layer, there was no expression of ERα in both groups. The expression of ERβ in the smooth muscle layer was nearly identical in the group of boys with inguinal hernia and in boys with unilateral cryptorchidism: no expression in 7 and 10 cases, normal expression in 32 and 34 cases, and high expression in 11 and 6 cases, respectively.

Figures 14 shows the expression of the alpha and beta receptors in the particular layers in both groups.


In this study we focused on ERα and ERβ expression in paratesticular tissues of cryptorchid testes. There are few reports about the relationship between ERs and spermatogenic failure in cryptorchidism [37,38]. It was shown that testosterone level was lower and estradiol level was higher in the cryptorchid than in normal testes by radioimmunological analysis of testicular tissue [37,39]. Studies in rodents have revealed that ERα is predominantly expressed in the pituitary, uterus, ovary, mammary gland, testis, epididymis and kidney; whereas ERβ is predominant in hypothalamus, prostate, lung, and bladder [40]. In our study we found expression of ERα and ERβ in the mesothelial layer, stromal cells, and the endothelial layer of paratesticular tissues of normal and undescended testes. In the smooth muscle layer there was no expression of ERα and nearly identical expression of ERβ. Mizuno et al showed increased expression of ERα in cryptorchid testes, suggesting that estradiol level was increased in the cryptorchid testes because estrogens upregulate the expression of the ERα gene in most mammalian tissues [37,41]. We also observed higher expression of ERα in the mesothelial layer of paratesticular tissues of undescended testes. In our study we found also higher expression of ERβ in the stromal cell layer of paratesticular tissue in undescended testes. Excess intratesticular estrogens inhibit spermiation [37,42]. An estrogen excess can decrease testicular androgen production by lowering the activity of steroidogenic enzymes that convert progesterone to testosterone [43]. The estrogens also act as permanent organizing agents during male fetal development, and as reversible regulators in adult life. Strauss et al. have mentioned the importance of androgen-estrogen balance for male fertility and reproductive tract function. Using transgenic male mice that express human aromatase, they demonstrated that chronic imbalance in the androgen-estrogen ratio leads to severe abnormalities in the development, structure, and function of mouse Leydig cells [37,44]. In vertebrates, estradiol also inhibits Leydig cell precursor development. By reducing the number or volume of Leydig cells in the developing testis, testosterone production is compromised, with impaired masculinization (undescended testis, hypospadias) and spermatogenic progression [45]. In estrogen-treated mice, the intra-abdominal position of the testes is due to the absence of Insl3 hormone, but not of androgens. Estrogens block the first phase of testicular descent (transabdominal descent), which is controlled hormonally by Insl3 [30]. As a possible alternative mechanism, other authors suggested that in utero exposure to diethylstilbestrol can probably induce resistance to AMH, which is responsible not only for the apoptosis of the Müllerian ducts, but also plays a role in testicular descent [46]. In contrast to ERβ mutant mice, testicular descent in ERα mutant mice was not affected by in utero exposure to estradiol. The transabdominal descent appeared to be completed [1]. Insl3 transcription was fully restored in the absence of ERα, but not in the absence of ERβ, even in the presence of saturating levels of exogenous estrogens, strongly suggesting that ERα mediates Insl3 down-regulation and subsequent cryptorchidism upon exposure to xenoestrogens in utero[1]. Estradiol inhibits testicular descent via ERα by acting directly on fetal Leydig cells. This fact correlates with ERα expression in Leydig cells. ERα is expressed in fetal Leydig cells until birth, whereas ERβ is present in gonocytes, Sertoli cells, and Leydig cells, and this receptor subtype appears to remain in these cells until birth [1,47]. It has been shown that endogenous estrogen physiologically inhibits steroidogenesis via ERα by acting directly on fetal Leydig cells [1,48]. ERα-deficient mice display higher levels of testicular testosterone due to hypertrophy of fetal Leydig cells, and increased expression of Star, Cyp17a1, and P450scc genes.

Unilateral cryptorchidism carries an increased risk of infertility in adulthood [32]. Up to 30% of men operated on in childhood for unilateral cryptorchidism are likely to be subfertile in later life [49]. Men who undergo an operation for bilateral cryptorchidism are more affected – up to 54% are infertile according to their semen and hormonal analysis [50]. The position of the testes at the time of orchidopexy is also important. In fact, a lack of fertility has been reported in men who underwent bilateral abdominal orchidopexy in childhood [51]. In our study, mean diameters of undescended testes were smaller in comparison to the normally developing ones (1×0.5 cm and 1.5×0.8 cm, respectively).

Testicular size and sperm density are positively correlated to germ-cell status in the cryptorchid testes in childhood [52]. Estrogenic exposure may, through ERα, inhibit the activation of Insl3 and steroidogenic genes in fetal Leydig cells.

If estrogen underlies sporadic cryptorchidism, then it is likely that these effects are mediated by smaller doses localized to the correct target tissue at the precise time, thus achieving maximal effect. It may be possible that a small excess of free estradiol at the right developmental stage may have a strong impact on testicular descent [30]. The main argument against estrogens as potential factors in impaired testicular descent is the lack of persistent Müllerian structures in affected humans [30].


Our results show that estrogens are potential mediators of cryptorchidism, and the inhibitory effects of estrogens on testicular descent may be mediated via ERα and ERβ.



Authors do not declare any conflict of interest.

fn9-medscimonit-18-10-cr630Source of support: Departmental sources


The authors of this article would like to give special thanks to Agnieszka Stewart for her invaluable editorial assistance.

1. Cederroth CR,Schaad O,Descombes P,et al. Estrogen receptor alpha is a major contributor to estrogen-mediated fetal testis dysgenesis and cryptorchidismEndocrinologyYear: 200714855071917673513
2. Baker LA,Nef S,Nguyen MT,et al. The insulin-3 gene: lack of a genetic basis for human cryptorchidismJ UrolYear: 2002167253411992081
3. Couse JF,Korach KS. Estrogen receptor null mice: what have we learned and where will they lead us?Endocr RevYear: 19992035841710368776
4. Pettersson K,Gustafsson JA. Role of estrogen receptor β in estrogen actionAnnu Rev PhysiolYear: 2001631659211181953
5. Henderson BE,Ross R,Bernstein L. Estrogens as a cause of human cancer: the Richard and Hinda Rosenthal Foundation award lectureCancer ResYear: 198848246532825969
6. Horowitz MC. Cytokines and estrogen in bone: anti-osteoporotic effectsScienceYear: 1993260626278480174
7. Akingbemi BT. Estrogen regulation of testicular functionRep Biol EndocrinolYear: 2005351
8. Jensen EV,Jacobson HI. Basic guides to the mechanism of estrogen actionRec Prog Horm ResYear: 196218387414
9. Kuiper GG,Gustafsson JA. The novel estrogen receptor-β subtype: potential role in the cell- and promoter-specific actions of estrogens and anti-estrogensFEBS LettYear: 199741087909247129
10. Mosselman S,Polman J,Dijkema R. ER β: identification and characterization of a novel human estrogen receptorFEBS LettYear: 199639249538769313
11. Tremblay GB,Tremblay A,Copeland NG,et al. Cloning, chromosomal localization, and functional analysis of the murine estrogen receptor βMol EndocrinolYear: 199711353659058381
12. Beato M. Gene regulation by steroid hormonesCellYear: 198956335442644044
13. Evans RM. The steroid and thyroid hormone receptor superfamilyScienceYear: 1988240889953283939
14. Zhao C,Dahlman-Wright K,Gustafsson JA. Estrogen receptor beta: an overview and updateNucl recept SignalYear: 20086e00318301783
15. Gill WB,Schumacher GF,Bibbo M,et al. Association of diethylstilbestrol exposure in utero with cryptorchidism, testicular hypoplasia and semen abnormalitiesJ UrolYear: 1979122363937351
16. Grocock CA,Charlton HM,Pike MC. Role of the fetal pituitary in cryptorchidism induced by exogenous maternal oestrogen during pregnancy in miceJ Reprod FertilYear: 1988832953002899644
17. Hadziselimovic F,Girard J. Pathogenesis of cryptorchidismHorm ResYear: 19778768320399
18. Hutson JM. Case of a testis prolapsed through a skin defect in the upper scrotumJ Pediatr SurgYear: 19922712571432544
19. Khan SA,Ball RB,Hendry WR. Effects of neonatal administration of diethylstilbestrol in male hamsters: Disruption of reproductive function in adults after apparently normal pubertal developmentBiol ReprodYear: 199858137429472934
20. Heyns CF,Hutson JM. Historical review of theories on testicular descentJ UrolYear: 1995153754677861531
21. Dorrington JH,Armstrong DT. Follicle stimulating hormone stimulates estradiol 17b synthesis in cultured Sertoli cellsProc Natl Acad Sci USAYear: 197572267781170613
22. Pomerantz DK. Developmental changes in the ability of FSH to stimulate estrogen synthesis in vivo by the testis of the ratBiol ReprodYear: 198023948546781544
23. Kelch RP,Jenner MR,Weinstein R,et al. Estradiol and testosterone secretion in human, simian and canine testes, in males with hypogonadism and in male pseudohermaphrodite with the feminizing testes syndromeJ Clin InvestYear: 197251824304259253
24. Nef S,Parada LF. Cryptorchidism in mice mutant for Insl3Nat GenetYear: 1999222959910391220
25. Zimmermann S,Steding G,Emmen JM,et al. Targeted disruption of the Insl3 gene causes bilateral cryptorchidismMol EndocrinolYear: 1999136819110319319
26. Hutson JM,Baker M,Terada M,et al. Hormonal control of testicular descent and the cause of cryptorchidismReprod Fertil DevYear: 19946151567991782
27. Hutson JM,Hasthorpe S,Heyns CF. Anatomical and functional aspects of testicular descent and cryptorchidismEndocr RevYear: 199718259809101140
28. Hutson JM,Hasthorpe S. Testicular descent and cryptorchidism: the state of the art in 2004J Pediatr SurgYear: 20054029730215750918
29. Adham IM,Agoulnik AI. Insulin-like 3 signalling in testicular descentInt J AndrolYear: 2004272576515379965
30. Nef S,Shipman T,Parada LF. A molecular basis for estrogen-induced cryptorchidismDev BiologyYear: 200022435461
31. Overbeek PA,Gorlov IP,Sutherland RW,et al. A transgenic insertion causing cryptorchidism in miceGenesisYear: 200130263511353515
32. Ferlin A,Bogatcheva NV,Gianeselto L. Insulin-like factor 3 gene mutations in testicular dysgenesis syndrome: clinical and functional characterizationMol Hum ReprodYear: 200612401616687567
33. Roh J,Virtanen H,Kumagai J. Lack of LGR8 gene mutation in Finnish patients with a family history of cryptorchidismReprod Biomed OnlineYear: 20037400614656401
34. Harnaen EJ,Na AF,Shenker NS. The anatomy of the cremaster muscle during inguinoscrotal testicular descent in the ratJ Pediatr SurgYear: 20074219828718082692
35. Foresta C,Zuccarello D,Garolla A,Ferlin A. Role of hormones, genes and environment in human cryptorchidismEndocrine ReviewsYear: 2008295608018436703
36. Nation TR,Balic A,Southwell BR. The hormonal control of testicular descentPed Endocrinol RevYear: 200972231
37. Mizuno K,Kojami Y,Kurosawa S,et al. Altered expression and localization of estrogen receptors Ralpha and beta In the testes of a cryptorchid rat modelUrologyYear: 201177251.e1e620951417
38. Li EZ,Li DX,Hang SQ,et al. 17-beta-estradiol stimulates proliferation of spermatogonia In experimental cryptorchid miceAsian J AndropYear: 2007965967
39. Hejmej A,Bilińska B. The effects of cryptorchidism on the regulation of steroidogenesis and gap junctional communication In equine testesEndokrynol PolYear: 2008591121818465685
40. Routledge EJ,White R,Parker MG,Sumptem JP. Differential effects of xenoestrogens on coactivator recruitment by estrogen receptor ER-α and ER-βJ Biol ChemYear: 2000275359869310964929
41. Robertson JA,Parnell Y,Lindhal LS,Ing NH. Estradiol up-regulates estrogen receptor Messenger ribonucleic acid In endometrial carcinoma cells by stabilizing the messageJ Mol EndocrinolYear: 2002291253512200234
42. D’Souza R,Pathak S,Upadhyay R,et al. Disruption of tubulobulbar complex by high intratesticular estrogens leading to failed spermiationEndocrinologyYear: 200915018616919095743
43. Smith EP,Boyd J,Frank GR,et al. Estrogen resistance caused by a mutation In the estrogen-receptor gene In a manN Engel J MedYear: 1994331105661
44. Strauss L,Kallio J,Desai N,et al. Increased exposure to estrogens disturbs maturation, steroidogenesis, and cholesterol homeostasis via estrogen receptor Ralpha In adult Mouse Leydig cellsEndocrinologyYear: 200915028657219196801
45. Hess RA,Buncik D,Lee KH,et al. A role for oestrogens In the male reproductive systemNatureYear: 1997390509129393999
46. Vidaeff AC,Sever LE. In utero exposure to environmental estrogens and male reproductive Heath: a systematic review of biological and epidemiologic evidenceReproductive ToxicologyYear: 20052052015808781
47. O’Donnell L,Robertson KM,Jones ME,Simpson ER. Estrogen and spermatogenesisEndor RevYear: 200022289318
48. Delbes G,Levacher C,Duquenne C,et al. Endogenous estrogens inhibit Mouse fetal Leydig cell development via estrogen receptor αEndocrinologyYear: 200514624546115661855
49. Thorup J,MaLachlan R,Cortes D,et al. What is new in cryptorchidism and hypospadias – a critical review on the testicular dysgenesis hypotesisJ Pediatr SurgYear: 20104520748620920735
50. Lee PA,Coughlin MT. Fertility after bilateral cryptorchidism. Evaluation by paternity, hormone and semen dataHorm ResYear: 200155283211423739
51. Taran I,Elder JS. Results of orchiopexy for the undescended testisWorld J UrolYear: 2006242313916676187
52. Hadziselimovic F,Hoecht B. Testicular histology related to fertility outcome and postpubertal hormone status in cryptorchidismKlin PädiatrYear: 2008220302718401814

Article Categories:
  • Clinical Research

Keywords: estrogen receptor, cryptorchidism, gonadal function, orchidopexy, testis descent.

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