FEMINIZED UPTAKE OF SEX STEROIDS IN THE HYPOTHALAMUS OF MALE RATS TREATED NEONATALLY WITH AN ANTI-ANDROGEN (CYPROTERONE)

1969 ◽  
Vol 61 (1_Suppl) ◽  
pp. S102
Author(s):  
Pentti Tuohimaa ◽  
Mikko Niemi
Keyword(s):  
Sex Steroids ◽  
Male Rats

Effects of Castration, Sex Steroids, LHRH and Glucocorticoids on LHRH Binding in the Anterior Pituitary of Male Rats

1982 ◽  
Vol 128 (1) ◽  
pp. 224-224
Author(s):  
O. Naess ◽  
L. Cusan ◽  
I. Brekke ◽  
K. Purvis ◽  
P. Torjesen ◽  
...  
Keyword(s):  
Sex Steroids ◽  
Anterior Pituitary ◽  
Male Rats

scholarly journals Effects of Sex Steroids on Secretory Granule Formation in Gonadotropes of Castrated Male Rats with Respect to Granin Expression*

Endocrinology ◽  
1998 ◽  
Vol 139 (6) ◽  
pp. 2765-2773 ◽  
Author(s):  
Tsuyoshi Watanabe ◽  
Tomohiro Banno ◽  
Thomas Jeziorowski ◽  
Yoshiyuki Ohsawa ◽  
Satoshi Waguri ◽  
...  
Keyword(s):  
Sex Steroids ◽  
Plasma Levels ◽  
Chromogranin A ◽  
Secretory Granules ◽  
Male Rats ◽  
Female Rat ◽  
Granule Formation ◽  
Male And Female ◽  
Immunocytochemical Studies ◽  
Circulating Levels

Abstract Pituitary gonadotropes show sex-related differences in their ultrastructure. Typical gonadotropes of male rats exhibit both large granules, which contain chromogranin A (CgA), and small granules, which contain secretogranin II (SgII). In contrast, typical female rat gonadotropes show only a very few large granules among the numerous small granules. To clarify the nature of the biogenesis of these secretory granules and the effects of sex steroids, the ultrastructural and immunocytochemical changes in gonadotropes were examined in castrated male rats supplied with a testosterone or estradiol implant. In castrated rats, pituitary expression and plasma levels of LH increased drastically, but the pituitary content of CgA decreased. The majority of gonadotropes then showed features of “castration cells” containing many small secretory granules. A testosterone implant to castrated rats remarkably suppressed the expression and circulating levels of LH and increased the CgA content in the pituitary to near-normal levels. In this situation, immunocytochemical studies demonstrated that gonadotropes again exhibited large and small secretory granules with the respective localization of CgA and SgII. On the contrary, in castrated rats supplied with an estradiol implant, the expression and content of CgA in the pituitary were remarkably suppressed, and large secretory granules disappeared from gonadotropes. These results suggest that the expression of CgA in gonadotropes is regulated differently by male and female sex steroids. These different effects of androgen and estrogen on the expression level of CgA are closely associated with the sex-related differences in the ultrastructure of secretory granules within gonadotropes.

scholarly journals Opposite Effects of Androgens and Estrogens on Adipogenesis in Rat Preadipocytes: Evidence for Sex and Site-Related Specificities and Possible Involvement of Insulin-Like Growth Factor 1 Receptor and Peroxisome Proliferator-Activated Receptorγ 21

Endocrinology ◽  
2000 ◽  
Vol 141 (2) ◽  
pp. 649-656 ◽  
Author(s):  
M. N. Dieudonne ◽  
R. Pecquery ◽  
M. C. Leneveu ◽  
Y. Giudicelli
Keyword(s):  
Growth Factor ◽  
Dehydrogenase Activity ◽  
Sex Steroids ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
17Β Estradiol ◽  
Glycerol 3 Phosphate Dehydrogenase

Abstract To investigate the role of sex steroid hormones in adipose tissue development and distribution, we have studied the effect of various sex steroids (testosterone, dihydrotestosterone (DHT), and 17β-estradiol) in vitro, on the proliferation and differentiation processes in rat preadipocytes from deep (epididymal and parametrial) and superficial (femoral sc) fat deposits. All added steroids failed to affect the growth rate of preadipocytes from male rats when determined from day 1 to day 4 after plating, whether FCS was present or not in the culture medium. In contrast, in preadipocytes from female rats, we observed a positive effect (×2) of 17β-estradiol (0.01μ m) on the proliferative capacities of sc but not parametrial preadipocytes. When preadipocytes were exposed to testosterone or DHT (0.1 μm) during the differentiation process, the glycerol 3-phosphate dehydrogenase activity was significantly decreased in epididymal preadipocytes only. When preadipocytes from male rats were exposed to 17β-estradiol (0.01μ m), the differentiation capacities of preadipocytes were not modified. However, in parametrial preadipocytes from ovariectomized female rats, 17β-estradiol significantly increased (×1.34) the glycerol 3-phosphate dehydrogenase activity. In differentiated preadipocytes that had been exposed to sex steroids, expression of peroxisome proliferator-activated receptor γ2 was up-regulated by 17β-estradiol but not by androgens. As described in other cell types, sex steroids modulate insulin growth factor 1 receptor (IGF1R) expression in preadipocytes. Indeed, IGF1R levels were either enhanced by 17 β-estradiol (0.01 μm) in sc preadipocytes from female ovariectomized rats or decreased by DHT (0.01 μm) in epididymal preadipocytes. These effects were reversed by simultaneous exposure to androgen or estrogen receptor antagonists. In conclusion, this study demonstrates that, in rat preadipocytes kept in primary culture and chronically exposed to sex hormones, androgens elicit an antiadipogenic effect, whereas estrogens behave as proadipogenic hormones. Moreover, our results suggest that these opposite effects could be related to changes in IGF1R (androgens and estrogens) and peroxisome proliferator-activated receptor γ2 expression (estrogens).

scholarly journals Effects of castration, sex steroids, LHRH and glucocorticoids on LHRH binding in the anterior pituitary of male rats

1981 ◽  
Vol 4 (1-6) ◽  
pp. 685-690 ◽  
Author(s):  
Oddvar Naess ◽  
Lionel Cusan ◽  
Inger Brekke ◽  
Kenneth Purvis ◽  
Peter Torjesen ◽  
...  
Keyword(s):  
Sex Steroids ◽  
Anterior Pituitary ◽  
Male Rats

scholarly journals PROFILE OF SEX STEROIDS AT EARLY STAGES OF LIVER METASTASIS FROM SARCOMA 45 IN MALE RATS

2017 ◽  
Vol 4 (1) ◽  
pp. 55-62
Author(s):  
I. V. Kaplieva ◽  
E. M. Frantsiyants ◽  
L. K. Trepitaki ◽  
N. D. Cheryarina
Keyword(s):  
Liver Metastasis ◽  
Sex Steroids ◽  
Male Rats ◽  
Early Stages ◽  
Sarcoma 45

scholarly journals Gender-Related Effects of Sex Steroids on Histamine Release and FcεRI Expression in Rat Peritoneal Mast Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Samira Muñoz-Cruz ◽  
Yolanda Mendoza-Rodríguez ◽  
Karen E. Nava-Castro ◽  
Lilián Yepez-Mulia ◽  
Jorge Morales-Montor
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Sex Steroids ◽  
Male Rats ◽  
Peritoneal Mast Cells ◽  
High Affinity Receptor ◽  
Ige Mediated ◽  
Affinity Receptor ◽  
And Gender ◽  
Pathologic Processes

Mast cells (MCs) are versatile effector and regulatory cells in various physiologic, immunologic, and pathologic processes. In addition to the well-characterized IgE/FcεRI-mediated degranulation, a variety of biological substances can induce MCs activation and release of their granule content. Sex steroids, mainly estradiol and progesterone, have been demonstrated to elicit MCs activation. Most published studies have been conducted on MCs lines or freshly isolated peritoneal and bone marrow-derived MC without addressing gender impact on MC response. Our goal was to investigate if the effect of estradiol, progesterone, testosterone, and dihydrotestosterone (DHT) on MCs may differ depending on whether female or male rats are used as MCs donors. Our results demonstrated that effect of sex steroids on MCs histamine release is dose- and gender-dependent and can be direct, synergistic, or inhibitory depending on whether hormones are used alone or to pretreat MCs followed by substance P-stimulation or upon IgE-mediated stimulation. In contrast, sex steroids did not have effect on the MC expression of the IgE high affinity receptor, FcεRI, no matter female or male rats were used. In conclusion, MCs degranulation is modulated by sex hormones in a gender-selective fashion, with MC from females being more susceptible than MC from males to the effects of sex steroids.

scholarly journals Role of Androgens in Sex Differences in Cardiac Damage During Myocardial Infarction

Endocrinology ◽  
2014 ◽  
Vol 155 (2) ◽  
pp. 568-575 ◽  
Author(s):  
Thi Y. L. Le ◽  
Anthony W. Ashton ◽  
Mahidi Mardini ◽  
Peter G. Stanton ◽  
John W. Funder ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sex Differences ◽  
Androgen Receptor ◽  
Sex Steroids ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
B Cell Lymphoma ◽  
Male Rats ◽  
Cardiac Damage

Age-specific incidence of ischemic heart disease in men is higher than in women, although women die more frequently without previous symptoms; the molecular mechanism(s) are poorly understood. Most studies focus on protection by estrogen, with less attention on androgen receptor-mediated androgen actions. Our aim was to determine the role of androgens in the sex differences in cardiac damage during myocardial infarction. Mature age-matched male and female Sprague Dawley rats, intact or surgically gonadectomized (Gx), received testosterone (T) or 17β-estradiol (E2) via subdermal SILASTIC (Dow Corning Corp.) implants; a subset of male rats received dihydrotestosterone. After 21 days, animals were anesthetized, and hearts were excised and subjected to ex vivo regional ischemia-reperfusion (I-R). Hearts from intact males had larger infarcts than those from females following I-R; Gx produced the opposite effect, confirming a role for sex steroids. In Gx males, androgens (dihydrotestosterone, T) and E2 aggravated I-R-induced cardiac damage, whereas in Gx females, T had no effect and E2 reduced infarct area. Increased circulating T levels up-regulated androgen receptor and receptor for advanced glycation end products, which resulted in enhanced apoptosis aggravating cardiac damage in both males and females. In conclusion, our study demonstrates, for the first time, that sex steroids regulate autophagy during myocardial infarction and shows that a novel mechanism of action for androgens during I-R is down-regulation of antiapoptotic protein Bcl-xL (B cell lymphoma-extra large), a key controller for cross talk between autophagy and apoptosis, shifting the balance toward apoptosis and leading to aggravated cardiac damage.

Effects of orchidectomy and sex steroids on vasopressin response to dehydration

1982 ◽  
Vol 99 (4) ◽  
pp. 493-499 ◽  
Author(s):  
G. Valiquette ◽  
L. Martini
Keyword(s):  
Sex Steroids ◽  
Water Deprivation ◽  
Gonadal Steroids ◽  
The Other ◽  
Male Rats ◽  
Sex Steroid ◽  
Short Term ◽  
Vasopressin Secretion ◽  
Hypothalamic Level

Abstract. The secretion of vasopressin has been shown recently to be influenced by gonadal steroids. To further evaluate the relevance of sex steroids in the control of vasopressin secretion, the vasopressin response to dehydration has been studied in normal, castrated and sex-steroid treated castrated male rats. Short-term (3 weeks) castration did not modify the vasopressin response to 48 h of water deprivation. Long-term (10 weeks) castration, on the other hand, consistently reduced the vasopressin response by more than 50%. In both cases, the osmolality was unaffected. Treatment of long-term castrated rats with testosterone, dihydrotestosterone, or oestradiol increased the vasopressin response to dehydration towards normal control levels. However, only oestradiol could restore it to and beyond normal levels, although all three steroids were given in doses that were equipotent in bringing back to normal the plasma LH levels of the castrated animals. Angiotensin-II generation may indirectly be augmented by oestradiol treatment and this may account for the effect of oestradiol here reported. No such mechanism, however, may be invoked in the case of androgens; a direct modulatory effect at the hypothalamic level is postulated for explaining their influence on vasopressin secretion.

Formation of DNA-adducts by selected sex steroids in rat liver

1996 ◽  
Vol 15 (7) ◽  
pp. 556-562 ◽  
Author(s):  
W. Feser ◽  
RS Kerdar H Blode ◽  
R. Reimann
Keyword(s):  
Rat Liver ◽  
Dna Adducts ◽  
Sex Steroids ◽  
Cyproterone Acetate ◽  
Adduct Formation ◽  
Dna Adduct ◽  
Male Rats ◽  
Female Rat ◽  
Chlormadinone Acetate

1 We are reporting investigations into the potential of the steroid hormones chlormadinone acetate (CMA), cyproterone acetate (CPA), ethinylestradiol (EE2) gestodene (GEST), megestrol acetate (MGA), norethis terone acetate (NET-Ac), estradiol (E 2), and progester one (P) to form DNA-adducts in rat liver in vivo. 2 Compound-related DNA-adduct spots were detected in male and female rat liver following CMA, CPA, and MGA using the 32P-postlabeling-technique. Substance- specific DNA-adducts were also observed in male rats after administration of E2. The other compounds showed no DNA-adduct formation. After treatment with CMA, CPA or MGA, the relative adduct labeling (RAL) differed sex- and substance-specifically.

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