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Journal articles on the topic 'Estrogenization'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Santti, Risto, Sari Mäkelä, Liisa Pylkkänen, Retha R. Newbold, and John A. McLachlan. "Developmental estrogenization and prostatic neoplasia." Prostate 24, no. 2 (February 1994): 67–78. http://dx.doi.org/10.1002/pros.2990240204.

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2

LONGHURST, PENELOPE A. "In Vitro Rat Bladder Function After Neonatal Estrogenization." Journal of Urology 168, no. 6 (December 2002): 2695–99. http://dx.doi.org/10.1016/s0022-5347(05)64246-2.

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3

Zurawa-Janicka, Dorota, Jaroslaw Kobiela, Tomasz Stefaniak, Agnieszka Wozniak, Joanna Narkiewicz, Michał Wozniak, Janusz Limon, and Barbara Lipinska. "Changes in expression of serine proteases HtrA1 and HtrA2 during estrogen-induced oxidative stress and nephrocarcinogenesis in male Syrian hamster." Acta Biochimica Polonica 55, no. 1 (January 30, 2008): 9–20. http://dx.doi.org/10.18388/abp.2008_3123.

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Serine proteases HtrA1 and HtrA2 are involved in cellular stress response and development of several diseases, including cancer. Our aim was to examine the involvement of the HtrA proteins in acute oxidative stress response induced in hamster kidney by estrogen treatment, and in nephrocarcinogenesis caused by prolonged estrogenization of male Syrian hamster. We used semi-quantitative RT-PCR to estimate the HtrA1 and HtrA2 mRNA levels in kidney tissues, and Western blotting to monitor the amount of the HtrA proteins. Within the first five hours following estrogen administration both HtrA1 mRNA and the protein levels were increased significantly. No changes in the expression of HtrA2 were observed. This indicates that HtrA1 may be involved in the response against oxidative stress induced by estrogen treatment in hamster kidney. During prolonged estrogenization, a significant reduction of the HtrA1 mRNA and protein levels was observed after 6 months of estradiol treatment, while the expression of HtrA2 was significantly elevated starting from the third month. This suggests an involvement of the HtrA proteins in estrogen-induced nephrocarcinogenesis in hamster. Using fluorescence in situ hybridization we localized the HtrA1 gene at the qb3-4 region of Syrian hamster chromosome 2, the region known to undergo a nonrandom deletion upon prolonged estrogenization. It is possible that the reduced level of HtrA1 expression is due to this chromosomal aberration. A full-length cDNA sequence of the hamster HtrA1 gene was obtained. It codes for a 50 kDa protein which has 98 and 96% identity with mouse and human counterparts, respectively.

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4

Saffarini, Camelia M., Elizabeth V. McDonnell-Clark, Ali Amin, and Kim Boekelheide. "A Human Fetal Prostate Xenograft Model of Developmental Estrogenization." International Journal of Toxicology 34, no. 2 (January 29, 2015): 119–28. http://dx.doi.org/10.1177/1091581815569364.

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Prostate cancer is a common disease in older men. Rodent models have demonstrated that an early and later-life exposure to estrogen can lead to cancerous lesions and implicated hormonal dysregulation as an avenue for developing future prostate neoplasia. This study utilizes a human fetal prostate xenograft model to study the role of estrogen in the progression of human disease. Histopathological lesions were assessed in 7-, 30-, 90-, 200-, and 400-day human prostate xenografts. Gene expression for cell cycle, tumor suppressors, and apoptosis-related genes (ie, CDKN1A, CASP9, ESR2, PTEN, and TP53) was performed for 200-day estrogen-treated xenografts. Glandular hyperplasia was observed in xenografts given both an initial and secondary exposure to estradiol in both 200- and 400-day xenografts. Persistent estrogenic effects were verified using immunohistochemical markers for cytokeratin 10, p63, and estrogen receptor α. This model provides data on the histopathological state of the human prostate following estrogenic treatment, which can be utilized in understanding the complicated pathology associated with prostatic disease and early and later-life estrogenic exposures.

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5

Kopylova, I. V., and M. A. Kareva. "Risk factors of impaired fertility in the patients presenting with congenital adrenal cortical hyperplasia." Problems of Endocrinology 59, no. 3 (June 15, 2013): 51–56. http://dx.doi.org/10.14341/probl201359351-56.

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The analysis of publications concerning the impairment of fertility in the patients presenting with congenital adrenal cortical hyperplasia was focused on the reduction of the degree of estrogenization. It included the data on the course of sexual development and the outcomes of feminizing plastic procedures in the girls suffering this disease depending on the degree of its compensation and the date of onset of the treatment.

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6

Lehtimaki, Jyrki, Sari Makela, Jaakko Viljamaa, Ahmed Yagi, Jorma Paranko, and Risto Santti. "Neonatal Estrogenization of the Male Mouse Results in Urethral Dysfunction." Journal of Urology 156, no. 6 (December 1996): 2098–103. http://dx.doi.org/10.1016/s0022-5347(01)65443-0.

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7

Aceitero, J., F. Gaytan, and F. B. Ranz. "Effects of neonatal estrogenization on rat bone development: A histomorphometric study." Calcified Tissue International 40, no. 4 (July 1987): 189–93. http://dx.doi.org/10.1007/bf02556620.

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8

MORALES-MONTOR, J., I. ARRIETA, L. I. DEL CASTILLO, M. RODRÍGUEZ-DORANTES, M. A. CERBÓN, and C. LARRALDE. "Remote sensing of intraperitoneal parasitism by the host's brain: regional changes of c-fos gene expression in the brain of feminized cysticercotic male mice." Parasitology 128, no. 3 (March 2004): 343–51. http://dx.doi.org/10.1017/s0031182003004529.

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Experimental intraperitoneal Taenia crassiceps cysticercosis in mice exhibits distinct genetical, immunological and endocrinological features possibly resulting from the complex interactive network of their physiological systems. Very notable is the tendency of parasites to grow faster in hosts of the female sex. It is also remarkable in the feminization process that the infection induces in chronically infected male mice, characterized by their estrogenization, deandrogenization and loss of sexual and aggressive patterns of behaviour. The proto-oncogene c-fos is a sex steroid-regulated transcription factor gene, expressed basally and upon stimulation by many organisms. In the CNS of rodents, c-fos is found expressed in association to sexual stimulation and to various immunological and stressful events. Hence, we suspected that changes in c-fos expression in the brain could be involved in the feminization of the infected male mice. Indeed, it was found that c-fos expression increased at different times during infection in the hypothalamus, hippocampus, less so in the preoptic area and cortex, and not in several other organs. The significant and distinctive regional changes of c-fos in the CNS of infected mice indicate that the brain of the host senses intraperitoneal cysticercosis and may also announce its active participation in the regulation of the host–parasite relationship. Possibly, the host's CNS activity is involved in the network that regulates the estrogenization and deandrogenization observed in the chronically infected male mice, as well as in the behavioural and immunological peculiarities observed in this parasitic infection.

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9

Prins, Gail S. "Developmental estrogenization: Prostate gland reprogramming leads to increased disease risk with aging." Differentiation 118 (March 2021): 72–81. http://dx.doi.org/10.1016/j.diff.2020.12.001.

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10

Soto, Pedro, Hilda María Echevarría, Cristina Esther Monteavaro, and María del Carmen Catena. "Experimentally induced intravaginal Tritrichomonas foetus infection in a mouse model." Pesquisa Veterinária Brasileira 25, no. 4 (December 2005): 225–30. http://dx.doi.org/10.1590/s0100-736x2005000400007.

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The interest to develop research on the host-parasite relationship in bovine tritrichomonosis has accomplished the use of experimental models alternative to cattle. The BALB/c mouse became the most appropriate species susceptible to vaginal Tritrichomonas foetus infection requiring previous estrogenization. For the need of an experimental model without persistent estrogenization and with normal estrous cycles, the establishment and persistence of vaginal infection on BALB/c mouse with different concentrations of T. foetus in two experimental groups was evaluated. Group A was treated with 5mg of b-estradiol 3-benzoate to synchronize the estrous, 48 hours before the T. foetus vaginal inoculation, and Group B was inoculated in natural estrus. At 5-7 days after treatment, estrogenic effect decreased allowing all animals to cycle regularly during the experiment. From the first week post-infection, samples of vaginal mucus were taken from all animals during 34 weeks, in order to evaluate the course of infection and the stage of the estrus cycle. Group A showed 93.6% of infected animals, and Group B showed 38%. Different doses of T. foetus were assayed to establish the vaginal infection, with a persistence of 34 weeks. Although different behavior was observed in each subgroup belonging to either Group A or Group B, there were no significant differences among the infecting doses used. The b-estradiol 3-benzoate treatment had a favorable effect on the establishment of the infection (P<0.0001), but it did not influence its persistence (P=0.1097). According to the results, an experimental mouse model is presented, appropriate for further studies on mechanisms of pathogenicity, immune response, protective evaluation of immunogen and therapeutic effect of drugs.

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11

Lindau, Stacy Tessler, Annie Dude, Natalia Gavrilova, Joscelyn N. Hoffmann, L. Philip Schumm, and Martha K. McClintock. "Prevalence and correlates of vaginal estrogenization in postmenopausal women in the United States." Menopause 24, no. 5 (May 2017): 536–45. http://dx.doi.org/10.1097/gme.0000000000000787.

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12

Masui, Fujiko, Keiko Kurosaki, Takao Mori, and Manabu Matsuda. "Persistent trefoil factor 1 expression imprinted on mouse vaginal epithelium by neonatal estrogenization." Cell and Tissue Research 323, no. 1 (August 30, 2005): 167–75. http://dx.doi.org/10.1007/s00441-005-0049-4.

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13

Cabral, C., L. Correa, F. Sampaio, and L. Cardoso. "298 Compositional changes in vesical extracellular matrix in male rats after neonatal estrogenization with diethylstilbestrol." European Urology Supplements 3, no. 2 (February 2004): 77. http://dx.doi.org/10.1016/s1569-9056(04)90297-7.

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14

Masui, Fujiko, Manabu Matsuda, and Takao Mori. "Involvement of keratinocyte growth factor (KGF)-KGF receptor signaling in developmental estrogenization syndrome of mouse vagina." Cell and Tissue Research 318, no. 3 (October 5, 2004): 591–98. http://dx.doi.org/10.1007/s00441-004-0980-9.

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15

Tena-Sempere, M., J. Navarro, L. Pinilla, LC Gonzalez, I. Huhtaniemi, and E. Aguilar. "Neonatal exposure to estrogen differentially alters estrogen receptor alpha and beta mRNA expression in rat testis during postnatal development." Journal of Endocrinology 165, no. 2 (May 1, 2000): 345–57. http://dx.doi.org/10.1677/joe.0.1650345.

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The biological actions of estrogens on target cells are mediated by two nuclear receptors: the estrogen receptor (ER) alpha and the recently characterized ER beta. In the male rat, the physiological role of estrogens involves multiple actions, from masculinization of brain areas related to reproductive function and sexual behavior to regulation of testicular development and function. Paradoxically, however, administration of high doses of estrogen during the critical period of neonatal differentiation results in an array of defects in the reproductive axis that permanently disrupt male fertility. The focus of this study was to characterize the effects and mechanism(s) of action of neonatal estrogenization on the pattern of testicular ER alpha and beta gene expression during postnatal development. To this end, groups of male rats were treated at day 1 of age with estradiol benzoate (500 microg/rat), and testicular ER alpha and ER beta mRNA levels were assayed by semi-quantitative RT-PCR from the neonatal period until puberty (days 1-45 of age). Furthermore, the expression of androgen receptor (AR) mRNA was evaluated, given the partially overlapping pattern of tissue distribution of ER alpha, ER beta and AR messages in the developing rat testis. In addition, potential mechanisms for neonatal estrogen action were explored. Thus, to discriminate between direct effects and indirect actions through estrogen-induced suppression of serum gonadotropins, the effects of neonatal estrogenization were compared with those induced by blockade of gonadotropin secretion with a potent LHRH antagonist in the neonatal period. Our results indicate that neonatal exposure to estrogen differentially alters testicular expression of alpha and beta ER messages: ER alpha mRNA levels, as well as those of AR, were significantly decreased, whereas relative and total expression levels of ER beta mRNA increased during postnatal/prepubertal development after neonatal estrogen exposure, a phenomenon that was not mimicked by LHRH antagonist treatment. It is concluded that the effect of estrogen on the expression levels of ER alpha and beta mRNAs probably involves a direct action on the developing testis, and cannot be attributed to estrogen-induced suppression of gonadotropin secretion during the neonatal period.

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16

Matsuda, Manabu, Fujiko Masui, and Takao Mori. "Neonatal estrogenization leads to increased expression of cellular retinol binding protein 2 in the mouse reproductive tract." Cell and Tissue Research 316, no. 1 (April 1, 2004): 131–39. http://dx.doi.org/10.1007/s00441-004-0852-3.

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17

Pinilla, L., M. Cocconi, S. Zoppi, and L. Martini. "Effect of neonatal estrogenization on testosterone metabolism in the prostate and in the epididymis of the rat." Journal of Steroid Biochemistry 32, no. 3 (March 1989): 459–65. http://dx.doi.org/10.1016/0022-4731(89)90222-7.

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18

Watanobe, Hajime, Shinsuke Sasaki, and Kazuo Takebe. "A comparative study of the effects of neonatal androgenization and estrogenization on prolactin secretion in adult female rats." Regulatory Peptides 34, no. 3 (July 1991): 149–58. http://dx.doi.org/10.1016/0167-0115(91)90174-f.

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19

Luo, Cheng, Leena Strauss, Ari Ristimäki, Tomi Streng, and Risto Santti. "Constant Expression of Cyclooxygenase-2 Gene in Prostate and the Lower Urinary Tract of Estrogen-Treated Male Rats." Zeitschrift für Naturforschung C 56, no. 5-6 (June 1, 2001): 455–63. http://dx.doi.org/10.1515/znc-2001-5-621.

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Expression of cyclooxygenase-2 (E. C. 1.14.99.1) in prostate and the lower urinary tract (LUT) of the neonatally estrogenized male rat has been studied by using a COX-2 ’s PCR fragment of 724 nt spanning 3 introns and a 478nt internal standard for quantitative RTPCR. The same fragment of 724 nt was used for RNA probe in Northern hybridization. Neonatal estrogenization (10 μg/day of diethylstilbestrol on days 1-5) had no effect on COX -2 expression in prostatic urethra, prostatic lobes, or bladder. Acute estrogen treatment of castrated animals did not induce COX-2 expression, either. In addition the differential expression of basal level of COX-2 in the different lobes of prostate in normal rat was demonstrated. Our results suggest a constant expression of COX-2 gene in prostate and the lower urinary tract of the neonatally estrogenized (neoDES) rats. The present study indicates that the increased expression of COX -2 is probably not essential for the estrogen-driven development of stromal inflammation or hyperplastic and dysplastic alterations in the prostate of neoDES rats.

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20

Velichko, N. F., N. O. Karpenko, E. M. Koreneva, E. E. Chistyakova, N. P. Smolenko, and V. О. Bondarenko. "THE EFFECT OF STRESS AND PHYTOESTROGENIZATION IN THE NEONATAL PERIOD ON THE FERTILITY OF ADULT MALE RATS." Fiziolohichnyĭ zhurnal 66, no. 4 (August 20, 2020): 37–45. http://dx.doi.org/10.15407/fz66.04.037.

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In the paper the significance of milk-feeding period for the formation of male reproductive health is experimentally shown. It has been found that the use of emotional stress and excessive phytoestrogenization, both separately and together, in male rats during breastfeeding leads to certain disorders of the reproductive system in adulthood. Modeled emotional stress or phytoestergenization on the principle of imprinting caused hyperostrogeny, androgen deficiency, changes in the ratio of androgenization/estrogenization in adulthood. The applied factors led to impaired spermatogenesis, inhibition of sexual activity, and decreased reproductive potential. In the stressed animals, the decrease in androgens was such that the testosterone levels did not differ from intact females. In the case of joint application of the factors in the suckling period, in adult male rats there were no clinically significant changes in the sperm count. The concentration of sex hormones corresponded to the physiological norm, sexual behavior was characterized by slightly differentiated changes. However, a 2.5-fold decrease in their fertility (or potential number of offspring) was critical and largest among all study groups. The latter indicates impaired spermatogenesis and the formation of defective sperm, that is, the problem of the parental genome, possibly epigenetic in nature.

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21

Khan, Wahid Ali, Arshi Malik, and Mohd Wajid Ali Khan. "Estrogenization of insulin by catecholestrogen produced high affinity autoantibodies and altered the normal function of insulin in type 1 diabetes." Life Sciences 256 (September 2020): 117910. http://dx.doi.org/10.1016/j.lfs.2020.117910.

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22

Ruhlen, Rachel L., Kembra L. Howdeshell, Jiude Mao, Julia A. Taylor, Franklin H. Bronson, Retha R. Newbold, Wade V. Welshons, and Frederick S. vom Saal. "Low Phytoestrogen Levels in Feed Increase Fetal Serum Estradiol Resulting in the “Fetal Estrogenization Syndrome” and Obesity in CD-1 Mice." Environmental Health Perspectives 116, no. 3 (March 2008): 322–28. http://dx.doi.org/10.1289/ehp.10448.

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23

Andel, R. A. Van, C. L. Franklin, M. C. St Claire, L. K. Riley, C. L. Besch-Williford, and R. R. Hook. "Lesions of Experimental Genital Tritrichomonas foetus Infections in Estrogenized BALB/c Mice." Veterinary Pathology 33, no. 4 (July 1996): 407–11. http://dx.doi.org/10.1177/030098589603300406.

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Ninety-seven BALB/c mice were inoculated intravaginally with 8.0 X 105 Tritrichomonas foetus organisms, using either isolate ATCC 30003 or field isolate MU Y22 2 days after estrogenization with 15 μg 17β-estradiol. Reproductive tracts were examined at several time points post-inoculation to determine gross and histologic responses to trichomonad infection as compared to estrogenized, uninfected control animals. The two isolates varied greatly in ability to maintain chronic infection; no ATCC 30003-inoculated animals remained culture-positive beyond 7 weeks post-inoculation, whereas MU Y22-inoculated animals were infected for greater than 26 weeks. Lesions were seen in 40-60% of animals prior to 10 weeks post-inoculation and included moderate uterine dilation and glandular atrophy, uterine gland abscesses, pyometra, intramural perivascular lymphoid infiltrates, and ovarian bursitis. The severity of lesions was independent of the T. foetus isolate. Lesions became more severe at 10 weeks post-inoculation, and at 10 and 26 weeks post-inoculation, lesions were seen in 60% and 75% of animals, respectively. In addition to lesions described above, epithelial changes were marked at these late necropsies, including ulceration, flattening, hypertrophy, and squamous metaplasia. The lesions seen in these mice closely resemble those described in natural bovine infection, suggesting that the estrogenized BALB/c mouse is an excellent model for study of bovine trichomoniasis.

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24

Asirvatham, Adlyne Reena, Karthik Balachandran, Packiamary Jerome, Vettriselvi Venkatesan, Teena Koshy, and Shriraam Mahadevan. "Clinical, biochemical and genetic characteristics of children with congenital adrenal hyperplasia due to 17α-hydroxylase deficiency." Journal of Pediatric Endocrinology and Metabolism 33, no. 8 (August 27, 2020): 1051–56. http://dx.doi.org/10.1515/jpem-2020-0050.

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AbstractObjectivesCongenital adrenal hyperplasia (CAH) is an autosomal recessive disorder, that could rarely be due to 17 α-hydroxylase deficiency (17αOHD) and/or 17,20 lyase deficiency. Mutation of CYP17A1 gene causes deficiency of glucocorticoids and androgens but excess of mineralocorticoids. Lack of genital ambiguity in most children causes a delay in diagnosis even until puberty. Classical presentation with hypertension and hypokalemia is often not encountered. We intended to study the clinical, biochemical and genetic characteristics of children diagnosed with CAH due to 17αOHD.MethodsThree children who were diagnosed with CAH due to 17αOHD in our institute and on follow up were included in this retrospective study. Clinical, biochemical and genetic characteristics of these children were retrieved and studied from electronic medical records.ResultsTwo children were genetic females and one was genetic male, but all three were raised as females. All had hypertension at diagnosis except one but none had hypokalemia. All of them had mutation in the CYP17A1 gene. The two females responded well to oestrogen and progesterone and had adequate estrogenization clinically.ConclusionsEven though CAH due to 17αOHD is quite rare, it should be considered while evaluating young individuals with hypogonadism, hypertension with or without hypokalemia. Lack of genital ambiguity and absence of classical signs at presentation does not rule out this not so uncommon condition and warrants follow up.

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25

Collado, Dolores, and Enrique Aguilar. "Further evidence that prolactin secretion in adult female rats is differently modified after neonatal estrogenization or androgenization: Responses to methysergide, quipazine, and pizotifen." Physiology & Behavior 53, no. 1 (January 1993): 161–65. http://dx.doi.org/10.1016/0031-9384(93)90025-b.

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26

Batubara, Jose R. L., Adji Suranto, Sudigdo Sastroasmoro, Bambang Tridjaja, and Aman B. Pulungan. "Natural history of premature thelarche: review of 60 girls." Paediatrica Indonesiana 41, no. 6 (December 31, 2001): 279. http://dx.doi.org/10.14238/pi41.6.2001.279-83.

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In Indonesia report on the natural history of premature thelarche is very limited. Daily practice requires physicians to have some basic practical knowledge, among others the natural history of premature thelarche, in order to manage these patients properly. We reviewed data of 85 premature thelarche patients who visited our department from January 1989 until December 1998. Only 60 patients met the study criteria. The mean chronological age of the patients at diagnosis was 43.4 months. About half of these patients (31/60) were diagnosed before they were 2 years old. Half of the patients had bilateral breast involvement. The hormonal pattern showed 24/48 follicle stimulating hormone predominant-response. Most patients (33/47) showed normal plasma estradiol level. Bone age analysis was normal in 46/57 patients, and only 9 showed accelerated bone age. Pelvic ultrasonography showed prepubertal reproduction organs in 26/35. Vaginal smears showed signs of estrogenization with various degree of stimulation in 13 patients. At the end of observation the outcome of premature thelarche were: 31 regressed, 19 persisted, 6 had progressive breast development and 4 progressed to central precocious puberty. The initial clinical and laboratory characteristics of those who developed CPP varied. Among 31 premature thelarche patients who regressed, 21 had onset of breast enlargement before age of 2 years. In most of the regressed patients (20/31), regression occurred completely within the first year. Most premature thelarche patients with onset before 2 years will regress within one year after diagnosis.

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Pisera, D., M. Candolfi, S. Navarra, J. Ferraris, V. Zaldivar, G. Jaita, M. G. Castro, and A. Seilicovich. "Estrogens sensitize anterior pituitary gland to apoptosis." American Journal of Physiology-Endocrinology and Metabolism 287, no. 4 (October 2004): E767—E771. http://dx.doi.org/10.1152/ajpendo.00052.2004.

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Tissue homeostasis results from a balance between cell proliferation and cell death by apoptosis. Estradiol affects proliferation as well as apoptosis in hormone-dependent tissues. In the present study, we investigated the apoptotic response of the anterior pituitary gland to lipopolysaccharide (LPS) in cycling female rats, and the influence of estradiol in this response in ovariectomized (OVX) rats. The OVX rats were chronically estrogenized with implanted Silastic capsules containing 1 mg of 17β-estradiol (E2). Cycling or OVX and E2-treated rats were injected with LPS (250 μg/rat ip). Apoptosis was determined by the terminal deoxynucleotidyl-mediated dUTP nick-end labeling (TUNEL) method in sections of the anterior pituitary gland and spleen. Chronic estrogenization induced apoptosis in the anterior pituitary gland. Acute endotoxemia triggered apoptosis of cells in the anterior pituitary gland of E2-treated rats but not of OVX rats. No differences were observed in the apoptotic response to LPS in spleen between OVX and E2-treated rats. The apoptotic response of the anterior pituitary to LPS was variable along the estrous cycle, being higher at proestrus than at estrus or diestrus I. Approximately 75% of the apoptotic cells were identified as lactotropes by immunofluorescence. In conclusion, our results indicate that estradiol induces apoptosis and enables the proapoptotic action of LPS in the anterior pituitary gland. Also, our study suggests that estrogens may be involved in anterior pituitary cell renewal during the estrous cycle, sensitizing lactotropes to proapoptotic stimuli.

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Watanobe, Hajime, and Kazuo Takebe. "A Comparative Study of the Effects of Neonatal Androgenization and Estrogenization on Vasoactive Intestinal Peptide Levels in the Anterior Pituitary and the Hypothalamus of Adult Female Rats." Neuroendocrinology 56, no. 5 (1992): 653–59. http://dx.doi.org/10.1159/000126289.

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29

Kopylova, I. V., V. Yu Sysoeva, T. M. Glybina, and M. A. Kareva. "Expression of estrogen and androgen receptors in tissues of external genitalia of girls with congenital adrenal hyperplasia." Problems of Endocrinology 60, no. 6 (December 15, 2014): 14–20. http://dx.doi.org/10.14341/probl201460614-20.

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The reason of post-operative introital stenosis in girls with CAH is a poor estrogenization of external genitalia before vaginoplasty. It is possible that the local sensitivity to estrogens can be reduced due to prenatal androgen excess in addition to inadequate compensation, which results to decrease of estrogens production by the ovaries. Objective. To determine the distribution of estrogen and androgen receptors in genital tissue, depending on the form of CAH, the degree of external virilization and serum levels of androgens. Material and methods. The waste surgical tissues obtained during routine feminizing genitoplasty (clitoro- and vaginoplasty) was used for immunohistochemical study of estrogen (α and β) and androgen receptors in girls with CAH (n=13 and n=8, respectively). Results. The expression of estrogen (α, β) and androgen receptors was determined in genital tissues of girls with CAH. There was no significant correlation between the number of immunopositive cells in the tissues of labia minora and vagina and the degree of virilization, as well as between the number of cells expressing the receptors and serum levels of androgens (testosterone, 17-hydroxyprogesterone). There was no difference in the expression of estrogen and androgen receptors between girls with salt-wasting and simple virilizing forms of CAH. The expression of estrogen receptor α in vaginal tissues was reduced in girls who underwent repeated vaginoplasty and were under preoperative local estrogen therapy in comparison to patients in whom the vaginoplasty was performed for the first time (p=0.045). Conclusion. The distribution of estrogen and androgen receptors in the labial and vaginal tissues in girls with CAH doesn’t depend on the form of disease, external virilization and serum levels of androgens. Girls undergoing repeated vaginoplasty may have a reduced sensitivity to local estrogen therapy due to decrease of estrogen receptors expression in the vaginal mucosa.

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30

Ruiz-Pino, F., V. M. Navarro, A. H. Bentsen, D. Garcia-Galiano, M. A. Sanchez-Garrido, P. Ciofi, R. A. Steiner, J. D. Mikkelsen, L. Pinilla, and M. Tena-Sempere. "Neurokinin B and the Control of the Gonadotropic Axis in the Rat: Developmental Changes, Sexual Dimorphism, and Regulation by Gonadal Steroids." Endocrinology 153, no. 10 (October 1, 2012): 4818–29. http://dx.doi.org/10.1210/en.2012-1287.

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Abstract Neurokinin B (NKB), encoded by Tac2 in rodents, and its receptor, NK3R, have recently emerged as important regulators of reproduction; NKB has been proposed to stimulate kisspeptin output onto GnRH neurons. Accordingly, NKB has been shown to induce gonadotropin release in several species; yet, null or even inhibitory effects of NKB have been also reported. The basis for these discrepant findings, as well as other key aspects of NKB function, remains unknown. We report here that in the rat, LH responses to the NK3R agonist, senktide, display a salient sexual dimorphism, with persistent stimulation in females, regardless of the stage of postnatal development, and lack of LH responses in males from puberty onward. Such dimorphism was independent of the predominant sex steroid after puberty, because testosterone administration to adult females failed to prevent LH responses to senktide, and LH responsiveness was not restored in adult males treated with estradiol or the nonaromatizable androgen, dihydrotestosterone. Yet, removal of sex steroids by gonadectomy switched senktide effects to inhibitory, both in adult male and female rats. Sexual dimorphism was also evident in the numbers of NKB-positive neurons in the arcuate nucleus (ARC), which were higher in adult female rats. This is likely the result of differences in sex steroid milieu during early periods of brain differentiation, because neonatal exposures to high doses of estrogen decreased ARC NKB neurons at later developmental stages. Likewise, neonatal estrogenization resulted in lower serum LH levels that were normalized by senktide administration. Finally, we document that the ability of estrogen to inhibit hypothalamic Tac2 expression seems region specific, because estrogen administration decreased Tac2 levels in the ARC but increased them in the lateral hypothalamus. Altogether, our data provide a deeper insight into relevant aspects of NKB function as major regulator of the gonadotropic axis in the rat, including maturational changes, sexual dimorphism, and differential regulation by sex steroids.

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Freyberger, A., Peter Andrews, Elke Hartmann, Rolf Eiben, Ingo Loof, U. Schmidt, M. Temerowski, et al. "Testing of endocrine active substances using an enhanced OECD test guideline 407: Experiences from studies on flutamide and ethinylestradiol." Pure and Applied Chemistry 75, no. 11-12 (January 1, 2003): 2483–89. http://dx.doi.org/10.1351/pac200375112483.

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Groups of five male and five female Wistar rats were treated by gavage with 0, 1, 10, and 100 mg/kg body weight (b.w.) flutamide (FLU) or 0.01, 0.05, and 0.2 mg/kg b.w. of ethinylestradiol (EE2) for at least 28 days according to an enhanced Organization for Economic Cooperation and Development (OECD) test guideline (TG) 407 to investigate which of the current and/or additional parameters would detect effects on the endocrine system and to provide data on intralaboratory variability. Two identical studies were performed in parallel on each compound. Common enhancements were determination of thyroid hormones (T3, T4) and thyroid stimulating hormone (TSH), of the stage of the estric cycle to ensure necropsy of females in diestrus, of the number and morphology of epididymal sperm, and of additional organ weights (e.g., male accessory sex organs, MASO) and histopathology of additional organs (e.g., pituitary, vagina). Endocrine-mediated findings consistently observed in these studies were decreased relative weights of MASO at 100 mg/kg FLU and at 0.2 mg/kg EE2, histological changes in pituitary and testes at > or = 10 mg/kg and in MASO, epididymis and adrenals at 100 mg/kg in FLU-treated males, histological changes in the mammary gland at > or = 0.05 mg/kg and in testes, MASO and adrenals at 0.2 mg/kg in EE2-treated males, estrogenization of uterus and vagina (despite necropsy in diestrus) at > or = 0.01 mg/kg EE2, and changes in the ovary at 0.2 mg/kg EE2. Spermatology was insensitive (EE2) or revealed changes only at the maximum tolerated dose (MTD). Determination of T3, T4, and TSH did not contribute to the detection of the endocrine effects (FLU) or provided equivocal results. Doubling the group size to 10 animals by combining the studies run in parallel did not increase the sensitivity of detection of endocrine-mediated effects above the level obtained by histopathological examination of groups of five animals. Only some of the proposed enhancements evaluated were helpful in detecting the endocrine-mediated effects of FLU and EE2. Evaluation of studies according to an enhanced TG 407 on 10 compounds with different endocrine activities will identify the most appropriate enhancements.

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Vlasenko, S., O. Zhulinska, and O. Yeroshenko. "Clinical and laboratory prognostic indicators for fertility in sheep." Naukovij vìsnik veterinarnoï medicini, no. 1(149) (May 30, 2019): 6–14. http://dx.doi.org/10.33245/2310-4902-2019-149-1-6-14.

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With the use of technology of artificial insemination in sheep farms are not yet defined criteria for assessing the full value of the preparation of females for insemination, and hence – the possibility of prediction and correction of their fertilization, which prevents the rational use of cryopreserved semen and ensuring the maximum reception of the offspring. We have proved the prognostic importance of fertilization of the morphofunctional state of the vulva and the vagina and the quality of mucus in sheep breeds during estrus. The material of the study was 327 sheep of ascanian breeding, which during the sexual intercourse before insemination examined the vulva, vagina and evaluated the estrus slime (number, color, consistency, presence of impurities, elasticity, electrical resistance, type of crystallization, protein content). The results of ultrasound diagnosis of pregnancy were determined by the fertility of sheep with different integral compositions of clinical and laboratory parameters. It has been established that in sheep, in which fertility in the first sexual cycle reached 65.1%, most often found a pink, moderately edematous vulva with clear mucus. In females with pale mucous membrane and insignificant amount of mucus, the effectiveness of inseminates declined to 53.3-58.0%. In a significant amount of estral mucus, the proportion of infertile animals increased twofold. At the same time, the selection of liquid, but cloudy, or thick mucus is a sign of an unfavorable prognosis, in which fertility decreases by 1.8-2.1 times (p <0.001). Dense, white, paste-like isolates were observed in a small number of sheep, mostly bright at the beginning of the anestral season. Low fertility in the first sexual hunting (35.5%) and a high multiplicity of repeated inseminations (29.0%) indicate that sheep with thick estral slime are only beginning to enter the sexual season, and this quality of secrecy indicates an inadequate estrogenization of the body. It was also found that in the infertile sheep during sexual hunting, the protein content of cervical mucus was 4.8 times higher, and the elasticity of mucus was reduced by 2.9 times. The most prevalent was the prognosis of average fertilization (53.3-58.0%), which was recorded in 62.9% of experimental sheep. The prognosis of high fertilization, which resulted in 62.5-65.1% of oseminins, was found in 27.8% of females. At the same time, the number of females with a fertility forecast at 40% was only 3.1%, and the prevalence of an unfavorable prognosis, in which fertility was the smallest (30.0-35.5%), reached 6.2%. Key words: sheep, askanian breeding, estrus, fertility prognosis, estral mucus, vulva, vagina, artificial insemination.

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Prins, Gail S., Lynn Birch, Helga Habermann, William Y. Chang, Christopher Tebeau, Oliver Putz, and Charles Bieberich. "Influence of neonatal estrogens on rat prostate development." Reproduction, Fertility and Development 13, no. 4 (2001): 241. http://dx.doi.org/10.1071/rd00107.

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Brief exposure of rodents to estrogens during early development alters prostate branching morphogenesis and cellular differentiation in a dose-dependant manner. If estrogenic exposures are high, these disturbances lead to permanent imprints of the prostate, which include reduced growth, differentiation defects of the epithelial cells, altered secretory function and reduced responsiveness to androgens in adulthood. This process, referred to as neonatal imprinting or developmental estrogenization, is associated with an increased incidence of prostatic lesions with aging, which include hyperplasia, inflammation and dysplasia. To better understand how early estrogenic exposures can permanently alter prostate growth and function and predispose the gland to neoplasia, the effects of estrogens on prostatic steroid receptors, cell–cell communication molecules and key developmental genes were examined. Transient and permanent alterations in the expression of prostatic androgen receptors, estrogen receptors α (ERα) and β, and retinoic acid receptors are observed. It is proposed that the estrogen-induced alterations in these critical transcription factors play a fundamental role in initiating prostatic growth and differentiation defects. Down-stream effects of the altered steroid receptor expression include disruption of TGFβ paracrine communication, altered expression of gap junction connexin molecules and loss of epithelial cadherin on epithelial cells. Additionally, specific disruptions in the expression of prostatic developmental genes are observed in response to neonatal estrogen. An extended developmental period of hoxa-13 expression, a lack of hoxd-13 increase with maturation, and an immediate and sustained suppression of hoxb-13 was noted within prostatic tissue. A transient decrease inNkx3.1 expression in the developing prostate was also observed. Thus subtle and overt alterations in Hox-13 and Nkx3.1 genes may be involved in the altered prostate phenotype in response to neonatal estrogen exposure. In summary, estrogen imprinting of the prostate gland is mediated through up-regulated levels of stromal ERα, which initiates alterations in steroid receptor expression within the developing gland. Rather than being an androgen-dominated process, as occurs normally, prostatic development is regulated by alternate steroids, including estrogens and retinoids, in the estrogenized animal. This, in turn, leads to disruptions in the coordinated expression of critical developmental genes including TGFβ, Hox-13 genes and Nkx3.1. Since a precise temporal expression pattern of these and other molecules is normally required for appropriate differentiation of the prostatic epithelium and stroma, the estrogen-initiated disruption in this pattern would lead to permanent differentiation defects of the prostate gland. It is hypothesized that these molecular and cellular changes initiated early in life predispose the prostate to the neoplastic state upon aging.

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Prins, Gail S., William Y. Chang, Yan Wang, and Richard B. van Breemen. "Retinoic Acid Receptors and Retinoids Are Up-Regulated in the Developing and Adult Rat Prostate by Neonatal Estrogen Exposure." Endocrinology 143, no. 9 (September 1, 2002): 3628–40. http://dx.doi.org/10.1210/en.2002-220184.

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Abstract Exposure to estrogens during the neonatal period interrupts rat prostatic development by reducing branching morphogenesis and by blocking epithelial cells from entering a normal differentiation pathway. Upon aging, ventral prostates exhibit extensive hyperplasia, dysplasia, and massive lymphocytic infiltrate, suggesting that neonatal estrogens may predispose the prostate gland to precancerous lesions. Vitamin A (retinol) and their derivatives (retinoic acids) are known key developmental regulators that bind and activate retinoic acid receptors (RARs). To evaluate whether neonatal estrogenization alters the sensitivity of the developing rat prostate to retinoids, RARα, -β, and -γ cellular localization and protein levels were analyzed over the course of development and into adulthood by immunocytochemistry and Western analysis, whereas mRNA levels were measured using RT-PCR. In addition, intraprostatic retinol and retinoic acid levels were quantitated on d 10 and 90 using HPLC-mass spectroscopy. Male rats were given 25 μg estradiol benzoate or oil on d 1, 3, and 5 of life, and prostatic complexes were removed on d 6, 10, 15, 30, and 90. The RARs localized to distinct cell populations: RARβ was expressed within basal epithelial cells, RARα was localized to differentiated luminal epithelial cells and smooth muscle cells, and RARγ was expressed within periductal stromal cells. Over the normal course of development, total protein and mRNA levels for the RARs declined, so that the adult prostate possessed the lowest amounts of RAR. Exposure to estrogens during the neonatal period resulted in an immediate and sustained increase in RARα levels and in the number of cells that expressed RARβ, whereas RARγ levels were unaffected. Western analysis confirmed that total prostatic RAR protein levels were significantly increased, whereas RT-PCR demonstrated that RARα and RARβ mRNA levels were markedly elevated in response to estrogenic exposure. The total prostatic retinol content was tripled by estrogenic exposure on d 10 and 90, indicating that the ability to retain retinoids within the prostate was permanently increased. Intraprostatic levels of 9-cis- and all-trans-retinoic acid levels were reduced on d 10, whereas 13-cis-retinoic acid levels were increased in response to estrogens. In the adult prostates of rats exposed neonatally to estrogen, total retinoic acid levels were doubled due to significant increases in both 9-cis- and 13-cis-retinoic acids compared with those in control prostates. In summary, levels of specific RARs and their activating ligands are increased in the prostate gland after neonatal estrogenic exposure, and this effect is permanent throughout the life of the animal. Thus, we hypothesize that alterations in morphogenesis as well as dysplasia in the adult prostate may be mediated in part through augmentation of transcriptional signals in the retinoid pathway.

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LONGHURST, PENELOPE A. "In Vitro Rat Bladder Function After Neonatal Estrogenization." Journal of Urology, December 2002, 2695–99. http://dx.doi.org/10.1097/00005392-200212000-00104.

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Lehtimaki, Jyrki, Sari Makela, Jaakko Viljamaa, Ahmed Yagi, Jorma Paranko, and Risto Santti. "Neonatal Estrogenization of the Male Mouse Results in Urethral Dysfunction." Journal of Urology, December 1996, 2098–103. http://dx.doi.org/10.1097/00005392-199612000-00057.

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Prins, Gail S. "Developmental estrogenization: Prostate gland reprogramming leads to increased disease risk with aging." Differentiation, January 2021. http://dx.doi.org/10.1016/j.diff.2020.12.001.

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Athonvarangkul, Diana, Hillary Wyeth Hosier, Brian Wojeck, and Silvio E. Inzucchi. "SAT-258 Surprising Transformation of a Microprolactinoma to a Macroprolactinoma." Journal of the Endocrine Society 4, Supplement_1 (April 2020). http://dx.doi.org/10.1210/jendso/bvaa046.1057.

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Abstract Background: Microprolactinomas are typically benign tumors that rarely become macroprolactinomas. We present a rare case of a microprolactinoma that, after discontinuation of dopamine agonist (DA) therapy, transformed into a macroprolactinoma over a period of 6 years.Clinical Case: A 16-year-old woman initially presented for evaluation of galactorrhea without menstrual irregularities and was found to have elevated prolactin (68 ng/ml, normal range: 0-20), and a 4 mm pituitary microadenoma on MRI imaging. The patient was otherwise asymptomatic and other pituitary hormone levels were normal. She was treated with DA therapy (cabergoline 0.50 mg/week) which normalized her PRL level and improved but did not completely resolve the galactorrhea. She was then lost to follow up for 6 years. During that time, she discontinued cabergoline, but was still able to conceive, delivering a healthy baby after 2 years and breastfed briefly. She re-presented to her gynecologist 4 years after delivery for galactorrhea and secondary amenorrhea, both persistent since childbirth. Re-evaluation at that time revealed a much higher PRL level (432 ng/ml) and significant interval growth of the previous microadenoma to a 2.6 cm macroadenoma, now with extension into the left cavernous sinus, suprasellar cistern, with mass effect on the optic chiasm. The patient was retreated with cabergoline up to 3 mg/week, with a near-normal PRL level being achieved at 9 months (28 ng/ml). Repeat MRI revealed modest decrease of the adenoma to 2.4 cm. Galactorrhea resolved with reduction in PRL. However, amenorrhea persisted. Estradiol (30 pg/mL, 19-357 pg/mL) was low normal with normal withdrawal bleeding to medroxyprogesterone (MPA) challenge indicating reasonable estrogenization. She was treated with MPA to achieve regular cyclic bleeding every 3 months. Conclusion: This is an unusual case demonstrating significant growth of a microprolactinoma, which is typically a stable/indolent neoplasm, to a macroprolactinoma with invasive features. Previous studies of untreated microprolactinomas have shown that they undergo only subtle to minimal growth over 3 to 6 years and none transformed to a macroprolactinoma despite significant rises in PRL levels. In this clinical case, given the 6 intervening years that had elapsed in between MRIs, we cannot determine whether this represented moderate, progressive growth during that period after the discontinuation of DA therapy or whether the tumor had grown during pregnancy with its known stimulatory effects from hyperestrogenemia. The patient will require close follow-up to ensure ongoing shrinkage or at least stability of the adenoma and ongoing control of her hyperprolactinemia.References:1. Fertility and sterility39, 753-760 (1983). 2. Dietemann, J.L et al. Neuroradiology25, 133-138 (1983). 3. Garcia, M.M et al. Journal of endocrinological investigation18, 450-455 (1995).

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